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BACKGROUND: Skin fibrosis affects the normal function of the skin. TGF-ß1 is a key cytokine that affects organ fibrosis. The latency-associated peptide (LAP) is essential for TGF-ß1 activation. We previously constructed and prepared truncated LAP (tLAP), and confirmed that tLAP inhibited liver fibrosis by affecting TGF-ß1. SPACE peptide has both transdermal and transmembrane functions. SPACE promotes the delivery of macromolecules through the stratum corneum into the dermis. This study aimed to alleviate skin fibrosis through the delivery of tLAP by SPACE. METHODS: The SPACE-tLAP (SE-tLAP) recombinant plasmid was constructed. SE-tLAP was purified by nickel affinity chromatography. The effects of SE-tLAP on the proliferation, migration, and expression of fibrosis-related and inflammatory factors were evaluated in TGF-ß1-induced NIH-3T3 cells. F127-SE-tLAP hydrogel was constructed by using F127 as a carrier to load SE-tLAP polypeptide. The degradation, drug release, and biocompatibility of F127-SE-tLAP were evaluated. Bleomycin was used to induce skin fibrosis in mice. HE, Masson, and immunohistochemistry were used to observe the skin histological characteristics. RESULTS: SE-tLAP inhibited the proliferation, migration, and expression of fibrosis-related and inflammatory factors in NIH-3T3 cells. F127-SE-tLAP significantly reduced ECM production, collagen deposition, and fibrotic pathological changes, thereby alleviating skin fibrosis. CONCLUSION: F127-SE-tLAP could increase the transdermal delivery of LAP, reduce the production and deposition of ECM, inhibit the formation of dermal collagen fibers, and alleviate the progression of skin fibrosis. It may provide a new idea for the therapy of skin fibrosis.
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Polietilenos , Polipropilenos , Dermatopatias , Fator de Crescimento Transformador beta , Animais , Camundongos , Bleomicina/efeitos adversos , Colágeno/metabolismo , Fibrose/tratamento farmacológico , Hidrogéis/química , Hidrogéis/farmacologia , Polietilenos/farmacologia , Polipropilenos/farmacologia , Transdução de Sinais , Fator de Crescimento Transformador beta/metabolismo , Fator de Crescimento Transformador beta1/metabolismo , Dermatopatias/induzido quimicamente , Dermatopatias/tratamento farmacológico , Dermatopatias/metabolismo , Proteínas Smad/efeitos dos fármacos , Proteínas Smad/metabolismo , Pele/efeitos dos fármacos , Pele/metabolismo , Pele/patologiaRESUMO
OBJECTIVES: To identify novel genetic elements facilitating the horizontal transfer of the oxazolidinone/phenicol resistance gene optrA and the pleuromutilin-lincosamide-streptogramin A resistance gene lsa(E) in Streptococcus suis. METHODS: The complete genomes of S. suis HB18 and two transconjugants were obtained using both the Illumina and Nanopore platforms. MICs were determined by broth microdilution. Inverse PCR was performed to identify circular forms of the novel unconventional circularizable structure (UCS), genomic island (GI) and integrative and conjugative element (ICE). Conjugation experiments assessed the transferability of optrA and lsa(E) genes in S. suis. RESULTS: S. suis HB18 carried a multiresistance gene cluster optrA-lsa(E)-lnu(B)-aphA-aadE-spw. This gene cluster, flanked by intact and truncated erm(B) in the same orientation, resided on a novel ICESsuHB18. Inverse PCR revealed the existence of a novel UCS, named UCS-optrAâ+âlsa(E), which could excise the gene cluster optrA-lsa(E)-lnu(B)-aphA-aadE-spw and one copy of erm(B) from ICESsuHB18. Two transconjugants with different characteristics were obtained. In transconjugant T-JH-GI, UCS-optrAâ+âlsa(E) excised from ICESsuHB18 inserted into the erm(B)-positive GI, designated GISsuHB18, generating the novel GISsuHB18-1. Meanwhile, in T-JH-ICE, genetic rearrangement events occurred in ICESsuHB18 and GISsuHB18, forming the novel ICESsuHB18-1. CONCLUSIONS: This is the first report demonstrating the functionally active UCS-optrAâ+âlsa(E) excising from ICESsuHB18 and inserting into the erm(B)-positive GISsuHB18 during the conjugation process. The location of optrA and lsa(E) on a multiresistance UCS enhances its persistence and dissemination.
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Autophagy is a self-renewal mechanism that maintains homeostasis and can promote tissue regeneration by regulating inflammation, reducing oxidative stress and promoting cell differentiation. The interaction between biomaterials and tissue cells significantly affects biomaterial-tissue integration and tissue regeneration. In recent years, it has been found that biomaterials can affect various processes related to tissue regeneration by regulating autophagy. The utilization of biomaterials in a controlled environment has become a prominent approach for enhancing the tissue regeneration capabilities. This involves the regulation of autophagy in diverse cell types implicated in tissue regeneration, encompassing the modulation of inflammatory responses, oxidative stress, cell differentiation, proliferation, migration, apoptosis, and extracellular matrix formation. In addition, biomaterials possess the potential to serve as carriers for drug delivery, enabling the regulation of autophagy by either activating or inhibiting its processes. This review summarizes the relationship between autophagy and tissue regeneration and discusses the role of biomaterial-based autophagy in tissue regeneration. In addition, recent advanced technologies used to design autophagy-modulating biomaterials are summarized, and rational design of biomaterials for providing controlled autophagy regulation via modification of the chemistry and surface of biomaterials and incorporation of cells and molecules is discussed. A better understanding of biomaterial-based autophagy and tissue regeneration, as well as the underlying molecular mechanisms, may lead to new possibilities for promoting tissue regeneration. Video Abstract.
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Autofagia , Materiais Biocompatíveis , Materiais Biocompatíveis/farmacologia , Materiais Biocompatíveis/química , Diferenciação CelularRESUMO
Diabetic kidney disease (DKD) is the main cause of end-stage renal disease, and its clinical manifestations are progressive proteinuria, decreased glomerular filtration rate, and renal failure. The injury and death of glomerular podocytes are the keys to DKD. Currently, a variety of cell death modes have been identified in podocytes, including apoptosis, autophagy, endoplasmic reticulum (ER) stress, pyroptosis, necroptosis, ferroptosis, mitotic catastrophe, etc. The signaling pathways leading to these cell death processes are interconnected and can be activated simultaneously or in parallel. They are essential for cell survival and death that determine the fate of cells. With the deepening of the research on the mechanism of cell death, more and more researchers have devoted their attention to the underlying pathologic research and the drug therapy research of DKD. In this paper, we discussed the podocyte physiologic role and DKD processes. We also provide an overview of the types and specific mechanisms involved in each type of cell death in DKD, as well as related targeted therapy methods and drugs are reviewed. In the last part we discuss the complexity and potential crosstalk between various modes of cell death, which will help improve the understanding of podocyte death and lay a foundation for new and ideal targeted therapy strategies for DKD treatment in the future.
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Diabetes Mellitus , Nefropatias Diabéticas , Podócitos , Humanos , Nefropatias Diabéticas/patologia , Podócitos/metabolismo , Podócitos/patologia , Morte Celular , Apoptose , Células Epiteliais/metabolismo , Diabetes Mellitus/metabolismoRESUMO
The goal of this research was to reveal the protective effect and mechanism of fibroblast growth factor-1 (FGF1) on oxidative stress injury of H9c2 cells induced by hydrogen peroxide (H2O2). The effects of various concentrations of H2O2 and FGF1 on the activity of H9c2 cells were analyzed by Real Time Cell Analysis (RTCA). The content of ROS, calcium ion, mitochondrial membrane potential and apoptosis were detected by fluorescence probe, the mRNA expression of Bcl-2, Bax and Caspase-3 were detected by real-time PCR to evaluate whether FGF1 has ability to resist the apoptosis of cardiomyocytes caused by oxidative damage. The results showed that the proliferation of H9c2 cells could be inhibited after being treated with 200 µM H2O2 for 12 h, and 100 µg/ml FGF1 could increase the proliferation rate of H9c2 cells, mitochondrial membrane potential and the mRNA expression of Bcl-2, and reduce the ROS accumulation, the level of apoptosis, the content of intracellular calcium and the mRNA expression of Bax and Caspase-3 caused by H2O2. The results showed that FGF1 could regulate oxidative stress by improving mitochondrial function and inhibit the H2O2-induced apoptosis in H9c2 cells.
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Apoptose/fisiologia , Fator 1 de Crescimento de Fibroblastos/metabolismo , Miócitos Cardíacos/patologia , Estresse Oxidativo/fisiologia , Animais , Cálcio/metabolismo , Linhagem Celular , Proliferação de Células/fisiologia , Fator 1 de Crescimento de Fibroblastos/administração & dosagem , Peróxido de Hidrogênio/administração & dosagem , Potencial da Membrana Mitocondrial/fisiologia , Mitocôndrias Cardíacas/metabolismo , Ratos , Espécies Reativas de Oxigênio/metabolismoRESUMO
The world's aging population continues to grow at an unprecedented rate. Consequently, age-related diseases including diabetes and diabetic complication, neurodegenerative disease, cardiovascular disease have become a health problem that cannot be ignored. The purpose of this review is to summarize the benefits of curcumin for age-related diseases, and present the molecular mechanisms for this effect. Curcumin-a natural plant extract, has received worldwide attention in recent years, due to its low toxicity, low cost and significant effects. It is derived from the spice turmeric and has been used in traditional medicine to improve diabetes. Many reports indicate that curcumin can regulate blood sugar levels, decrease blood pressure, protect nerve cells, and enhance immunity. In addition, there is evidence for its antioxidant, anti-infective, anti-inflammatory, as well as promoting wound recovery, which suggests that curcumin may be especially beneficial for the elderly.
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Envelhecimento , Curcumina/farmacologia , Fatores Etários , Idoso , Animais , Anti-Inflamatórios não Esteroides/farmacologia , Antioxidantes/farmacologia , HumanosRESUMO
Diabetic nephropathy (DN) is a common cause of end-stage kidney disease (ESKD) all over the world. Sitagliptin, an inhibitor of DPP-IV plays a beneficial role in type 2 diabetic nephropathy. The purpose of this study was to explore the effect and mechanism of sitagliptin on renal injury in type 1 diabetic mice. Streptozotocin (STZ) induced type 1 diabetic mice were treated with oral administration of sitagliptin (15 mg/kg/ day) for 4 weeks. The results showed that sitagliptin treatment did not change the levels of blood glucose in STZ induced type 1 diabetic mice. Sitagliptin attenuates diabetic nephropathy by significantly inhibiting 24 h proteinuria, renal injury and fibrosis. Sitagliptin can inhibit the expression level of TGF-ß1 and the other related fibrosis factors in renal tissue of type 1 diabetic mice while delaying the progression of type 1 diabetic nephropathy. These results indicated that sitagliptin treatment is potentially a new strategy for treating type 1 diabetic nephropathy.
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Diabetes Mellitus Experimental/tratamento farmacológico , Diabetes Mellitus Tipo 1/tratamento farmacológico , Nefropatias Diabéticas/prevenção & controle , Inibidores da Dipeptidil Peptidase IV/farmacologia , Fosfato de Sitagliptina/farmacologia , Administração Oral , Animais , Glicemia/efeitos dos fármacos , Diabetes Mellitus Experimental/complicações , Diabetes Mellitus Tipo 1/complicações , Hipoglicemiantes/farmacologia , Masculino , Camundongos , Proteinúria/prevenção & controle , Transdução de Sinais/efeitos dos fármacos , Proteínas Smad/metabolismo , Estreptozocina , Fator de Crescimento Transformador beta1/genéticaRESUMO
The lack of antibacterial activity and the leaching of Ni ions seriously limit the potential applications of the near equiatomic nickel-titanium (NiTi) alloy in the biomedical field. In this study, a silver nanoparticles (Ag NPs) wrapped in a polydopamine (Ag@PDA) film modified NiTi alloy with controllable antibacterial activity and enhanced corrosion resistance was achieved using a one-pot approach in a mixed solution of AgNO3 and dopamine. The controllable antibacterial activity could be achieved by adjusting the initial concentration of dopamine (Cdop), which obtained Ag@PDA films with varying thickness of polydopamine layers coated on Ag NPs, thereby conferring different levels of antibacterial activity to the modified NiTi alloy. In vitro antibacterial ratios (24 h) of Ag@PDA film-modified NiTi alloy against E.coli and S.aureus ranged from 46 % to 100 % and from 42 % to 100 %, respectively. The release curves of Ag ions indicated the persistent antibacterial effect of Ag@PDA film-modified NiTi alloy for at least 21 days. Moreover, in vitro cytotoxicity and in vivo implantation tests demonstrated the satisfactory biosafety of the Ag@PDA film-modified NiTi alloy when used as bioimplants. This research offers valuable insight into meeting various antibacterial demands for NiTi alloy implantations and highlights the potential of Ag-containing film-modified biomaterials in addressing different types of infections induced by implantations.
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Diabetic wounds pose a significant challenge to public health, primarily due to insufficient blood vessel supply, bacterial infection, excessive oxidative stress, and impaired antioxidant defenses. The aforementioned condition not only places a significant physical burden on patients' prognosis, but also amplifies the economic strain on the medical system in treating diabetic wounds. Currently, the effectiveness of available treatments for diabetic wounds is limited. However, there is hope in the potential of metal nanoparticles (MNPs) to address these issues. MNPs exhibit excellent anti-inflammatory, antioxidant, antibacterial and pro-angiogenic properties, making them a promising solution for diabetic wounds. In addition, MNPs stimulate the expression of proteins that promote wound healing and serve as drug delivery systems for small-molecule drugs. By combining MNPs with other biomaterials such as hydrogels and chitosan, novel dressings can be developed and revolutionize the treatment of diabetic wounds. The present article provides a comprehensive overview of the research progress on the utilization of MNPs for treating diabetic wounds. Building upon this foundation, we summarize the underlying mechanisms involved in diabetic wound healing and discuss the potential application of MNPs as biomaterials for drug delivery. Furthermore, we provide an extensive analysis and discussion on the clinical implementation of dressings, while also highlighting future prospects for utilizing MNPs in diabetic wound management. In conclusion, MNPs represent a promising strategy for the treatment of diabetic wound healing. Future directions include combining other biological nanomaterials to synthesize new biological dressings or utilizing the other physicochemical properties of MNPs to promote wound healing. Synthetic biomaterials that contain MNPs not only play a role in all stages of diabetic wound healing, but also provide a stable physiological environment for the wound-healing process.
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Diabetes Mellitus , Nanopartículas Metálicas , Humanos , Antioxidantes , Materiais Biocompatíveis/química , Nanopartículas Metálicas/uso terapêutico , Nanopartículas Metálicas/química , Antibacterianos/uso terapêutico , Antibacterianos/química , Tecnologia , Hidrogéis/químicaRESUMO
Accumulating evidence indicates that cellular premature senescence of the glomerulus, including endothelial cells, mesangial cells, and podocytes leads to diabetic nephropathy (DN), and DN is regarded as a clinical model of premature senescence. However, the role of cellular senescence-associated genes in the glomerulus in DN progression remains unclear. Therefore, this work aims to identify and validate potential cellular aging-related genes in the glomerulus in DN to provide novel clues for DN treatment based on anti-aging. The microarray GSE96804 dataset, including 41 diabetic glomeruli and 20 control glomeruli, is retrieved from the Gene Expression Omnibus (GEO) database and cellular senescence-related genes (CSRGs) are obtained from the GeneCards database and literature reports. Subsequently, PPI, GO, and KEGG enrichment are analyzed by screening the intersection between differentially expressed genes (DEGs) and CSRGs. scRNA-seq dataset GSE127235 is used to verify core genes expression in glomerulocytes of mice. Finally, db/db mice are utilized to validate the hub gene expression in the glomeruli, and high glucose-induced mesangial cells are used to confirm key gene expression. This study reveals that FOS and ZFP36 may play an anti-aging role in DN to ameliorate cell intracellular premature aging in mesangial cells of glomeruli.
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Diabetes Mellitus , Nefropatias Diabéticas , Camundongos , Animais , Nefropatias Diabéticas/genética , Nefropatias Diabéticas/metabolismo , Nefropatias Diabéticas/prevenção & controle , Multiômica , Células Endoteliais/metabolismo , Glomérulos Renais/metabolismo , Camundongos Endogâmicos , Senescência Celular/genética , Diabetes Mellitus/metabolismoRESUMO
Diabetic wound healing remains a worldwide challenge for both clinicians and researchers. The high expression of matrix metalloproteinase 9 (MMP9) and a high inflammatory response are indicative of poor diabetic wound healing. H8, a curcumin analogue, is able to treat diabetes and is anti-inflammatory, and our pretest showed that it has the potential to treat diabetic wound healing. However, H8 is highly expressed in organs such as the liver and kidney, resulting in its unfocused use in diabetic wound targeting. (These data were not published, see Table S1 in the Supporting Information.) Accordingly, it is important to pursue effective carrier vehicles to facilitate the therapeutic uses of H8. The use of H8 delivered by macrophage membrane-derived nanovesicles provides a potential strategy for repairing diabetic wounds with improved drug efficacy and fast healing. In this study, we fabricated an injectable gelatin microsphere (GM) with sustained MMP9-responsive H8 macrophage membrane-derived nanovesicles (H8NVs) with a targeted release to promote angiogenesis that also reduces oxidative stress damage and inflammation, promoting diabetic wound healing. Gelatin microspheres loaded with H8NV (GMH8NV) stimulated by MMP9 can significantly facilitate the migration of NIH-3T3 cells and facilitate the development of tubular structures by HUVEC in vitro. In addition, our results demonstrated that GMH8NV stimulated by MMP9 protected cells from oxidative damage and polarized macrophages to the M2 phenotype, leading to an inflammation inhibition. By stimulating angiogenesis and collagen deposition, inhibiting inflammation, and reducing MMP9 expression, GMH8NV accelerated wound healing. This study showed that GMH8NVs were targeted to release H8NV after MMP9 stimulation, suggesting promising potential in achieving satisfactory healing in diabetic treatment.
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Diabetes Mellitus Experimental , Gelatina , Camundongos , Animais , Gelatina/farmacologia , Gelatina/química , Microesferas , Metaloproteinase 9 da Matriz/farmacologia , Metaloproteinase 9 da Matriz/uso terapêutico , Diabetes Mellitus Experimental/tratamento farmacológico , Cicatrização , Inflamação , MacrófagosRESUMO
Fabrication of versatile hydrogels in a facile and effective manner represents a pivotal challenge in the field of biomaterials. Herein, a novel strategy is presented for preparing on-demand degradable hydrogels with multilevel responsiveness. By employing selenol-dichlorotetrazine nucleophilic aromatic substitution (SNAr) to synthesize hydrogels under mild conditions in a buffer solution, the necessity of additives or posttreatments can be obviated. The nucleophilic and redox reactions between selenol and tetrazine culminate in the formation of three degradable chemical bonds-diselenide, aryl selenide, and dearomatized selenide-in a single, expeditious step. The resultant hydrogel manifests exceptional adaptability to intricate environments in conjunction with self-healing and on-demand degradation properties. Furthermore, the resulting material demonstrated light-triggered antibacterial activity. Animal studies further underscore the potential of integrating metformin into Se-Tz hydrogels under green light irradiation, as it effectively stimulates angiogenesis and collagen deposition, thereby fostering efficient wound healing. In comparison to previously documented hydrogels, Se-Tz hydrogels exhibit controlled degradation and drug release, outstanding antibacterial activity, mechanical robustness, and bioactivity, all without the need for costly and intricate preparation procedures. These findings underscore Se-Tz hydrogels as a safe and effective therapeutic option for diabetic wound dressings.
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Antibacterianos , Hidrogéis , Cicatrização , Cicatrização/efeitos dos fármacos , Hidrogéis/química , Animais , Camundongos , Antibacterianos/farmacologia , Antibacterianos/química , Materiais Biocompatíveis/química , Materiais Biocompatíveis/farmacologia , Modelos Animais de DoençasRESUMO
Diabetes is a common chronic metabolic disease, and its incidence continues to increase year after year. Diabetic patients mainly die from various complications, with the most common being diabetic cardiomyopathy. However, the detection rate of diabetic cardiomyopathy is low in clinical practice, and targeted treatment is lacking. Recently, a large number of studies have confirmed that myocardial cell death in diabetic cardiomyopathy involves pyroptosis, apoptosis, necrosis, ferroptosis, necroptosis, cuproptosis, cellular burial, and other processes. Most importantly, numerous animal studies have shown that the onset and progression of diabetic cardiomyopathy can be mitigated by inhibiting these regulatory cell death processes, such as by utilizing inhibitors, chelators, or genetic manipulation. Therefore, we review the role of ferroptosis, necroptosis, and cuproptosis, three novel forms of cell death in diabetic cardiomyopathy, searching for possible targets, and analyzing the corresponding therapeutic approaches to these targets.
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Diabetes mellitus is a metabolic disease that is characterized by chronic hyperglycemia due to a variety of etiological factors. Long-term metabolic stress induces harmful inflammation leading to chronic complications, mainly diabetic ophthalmopathy, diabetic cardiovascular complications and diabetic nephropathy. With diabetes complications being one of the leading causes of disability and death, the use of anti-inflammatories in combination therapy for diabetes is increasing. There has been increasing interest in targeting significant regulators of the inflammatory pathway, notably receptor-interacting serine/threonine-kinase-1 (RIPK1) and receptor-interacting serine/threonine-kinase-3 (RIPK3), as drug targets for managing inflammation in treating diabetes complications. In this review, we aim to provide an up-to-date summary of current research on the mechanism of action and drug development of RIPK1 and RIPK3, which are pivotal in chronic inflammation and immunity, in relation to diabetic complications which may be benefit for explicating the potential of selective RIPK1 and RIPK3 inhibitors as anti-inflammatory therapeutic agents for diabetic complications.
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Complicações do Diabetes , Diabetes Mellitus , Nefropatias Diabéticas , Humanos , Inflamação/tratamento farmacológico , Inflamação/metabolismo , Complicações do Diabetes/tratamento farmacológico , Proteína Serina-Treonina Quinases de Interação com Receptores/metabolismo , Treonina , Serina , Diabetes Mellitus/tratamento farmacológico , Diabetes Mellitus/etiologiaRESUMO
OBJECTIVES: This study aimed to investigate the feasibility of measuring the soft tissue height of bone cristae around implant by digital method. METHODS: A total of 36 patients with dental implants were selected from the Dental Medicine Center of the First Affiliated Hospital of University of Science and Technology of China (Anhui Provincial Hospital) from August 2022 to December 2022. A total of 43 dental implants were enrolled. All postoperative cone beam CT (CBCT) imaging data and intraoral digital impressions obtained before surgery were immediately obtained by the patients on the day of completion of oral implant surgery and they were imported into oral implant surgery planning software for image fitting. Then, virtual implants of the same specification were placed in the planting area, and the implant position was adjusted to overlap with the implant shadow in the CBCT image. Supracrestal tissue height (STH) was measured at the implant view interface (digital group). During the operation, implant holes were prepared step by step in accordance with the standard preparation method, and implants were implanted. The upper edge of the implant was flushed with the crest of the alveolar ridge. STH was measured by perio-dontal probing (periodontal probe group). Paired t-test was used to compare the STH differences between the digital and periodontal probe groups. Bland-Altman test was used to analyze the consistency of the two methods. Intra-group correlation coefficient (ICC) was used to verify the reliability of the results measured by different surveyors using di-gital methods. RESULTS: No statistical significance was observed in the STH difference between the two methods (P>0.05). Bland-Altman test showed good consistency between the two methods, but the measurement of mandibular posterior teeth showed that the results of periodontal probe were greater than those of digital method. The ICC and 95%CI of the STH results measured digitally by different surveyors are 0.992 (0.986-0.996). CONCLUSIONS: The digital me-thod is in good agreement with the periodontal probe method in measuring the soft tissue height of the bone cristae around the implant.
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Processo Alveolar , Implantes Dentários , Dente , Humanos , Processo Alveolar/diagnóstico por imagem , Tomografia Computadorizada de Feixe Cônico/métodos , Estudos de Viabilidade , Reprodutibilidade dos Testes , Dente/diagnóstico por imagemRESUMO
Solar-driven water evaporation is essential to provide sustainable and ecofriendly sources of fresh water. However, there are still great challenges in preparing materials with broadband light absorption for high photothermal efficiency as well as in designing devices with large evaporation areas and small heat dissipation areas to boost the water evaporation rate. We designed a hanging-mode solar evaporator based on the polyaniline/carbon nanotube (PANI/CNT) fabric, in which the photothermal fabric acts as the solar evaporator and the micropores on the cotton fabric act as the water transfer channels. The hanging mode provides efficient evaporation at both interfaces by greatly reducing the heat dissipation area. The hanging mode PANI/CNT fabric solar evaporator can achieve an evaporation rate of 2.81 kg·m-2·h-1 and a photothermal efficiency of 91.74% under a solar illumination of 1 kW·m-2. This high-performance evaporator is designed by regulating the photothermal material and evaporation device, which provides a novel strategy for sustainable desalination.
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Diabetic nephropathy (DN) is a chronic inflammatory disease that affects millions of diabetic patients worldwide. The key to treating of DN is early diagnosis and prevention. Once the patient enters the clinical proteinuria stage, renal damage is difficult to reverse. Therefore, developing early treatment methods is critical. DN pathogenesis results from various factors, among which the immune response and inflammation play major roles. Ferroptosis is a newly discovered type of programmed cell death characterized by iron-dependent lipid peroxidation and excessive ROS production. Recent studies have demonstrated that inflammation activation is closely related to the occurrence and development of ferroptosis. Moreover, hyperglycemia induces iron overload, lipid peroxidation, oxidative stress, inflammation, and renal fibrosis, all of which are related to DN pathogenesis, indicating that ferroptosis plays a key role in the development of DN. Therefore, this review focuses on the regulatory mechanisms of ferroptosis, and the mutual regulatory processes involved in the occurrence and development of DN and inflammation. By discussing and analyzing the relationship between ferroptosis and inflammation in the occurrence and development of DN, we can deepen our understanding of DN pathogenesis and develop new therapeutics targeting ferroptosis or inflammation-related regulatory mechanisms for patients with DN.
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Diabetes Mellitus , Nefropatias Diabéticas , Ferroptose , Humanos , Nefropatias Diabéticas/patologia , Estresse Oxidativo , Rim/patologia , Inflamação/metabolismo , Diabetes Mellitus/metabolismoRESUMO
Diabetic nephropathy (DN) is a prevalent chronic microvascular complication associated with diabetes mellitus and represents a major cause of chronic kidney disease and renal failure. Current treatment strategies for DN primarily focus on symptom alleviation, lacking effective approaches to halt or reverse DN progression. Circular RNA (circRNA), characterized by a closed-loop structure, has emerged as a novel non-coding RNA regulator of gene expression, attributed to its conservation, stability, specificity, and multifunctionality. Dysregulation of circRNA expression is closely associated with DN progression, whereby circRNA impacts kidney cell injury by modulating cell cycle, differentiation, cell death, as well as influencing the release of inflammatory factors and stromal fibronectin expression. Consequently, circRNA is considered a predictive biomarker and a potential therapeutic target for DN. This review provides an overview of the latest research progress in the classification, functions, monitoring methods, and databases related to circRNA. The paper focuses on elucidating the impact and underlying mechanisms of circRNA on kidney cells under diabetic conditions, aiming to offer novel insights into the prevention, diagnosis, and treatment of DN.
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Diabetes Mellitus , Nefropatias Diabéticas , Humanos , Nefropatias Diabéticas/diagnóstico , Nefropatias Diabéticas/genética , Nefropatias Diabéticas/terapia , RNA Circular/genética , RNA Circular/metabolismo , Rim/metabolismo , Biomarcadores/metabolismo , Diabetes Mellitus/metabolismoRESUMO
Diabetic nephropathy (DN) and diabetic retinopathy (DR) are the most serious and common diabetes-associated complications. DN and DR are all highly prevalent and dangerous global diseases, but the underlying mechanism remains to be elucidated. Ferroptosis, a relatively recently described type of cell death, has been confirmed to be involved in the occurrence and development of various diabetic complications. The disturbance of cellular iron metabolism directly triggers ferroptosis, and abnormal iron metabolism is closely related to diabetes. However, the molecular mechanism underlying the role of ferroptosis in DN and DR is still unclear, and needs further study. In this review article, we summarize and evaluate the mechanism of ferroptosis and its role and progress in DN and DR, it provides new ideas for the diagnosis and treatment of DN and DR.
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Diabetes Mellitus , Nefropatias Diabéticas , Retinopatia Diabética , Ferroptose , Doenças Retinianas , Humanos , Nefropatias Diabéticas/etiologia , Retinopatia Diabética/etiologia , FerroRESUMO
Autophagy, a self-renewal mechanism, can help to maintain the stability of the intracellular environment of organisms. Autophagy can also regulate several cellular functions and is strongly related to the onset and progression of several diseases. Wound healing is a biological process that is coregulated by different types of cells. However, it is troublesome owing to prolonged treatment duration and poor recovery. In recent years, biomaterials have been reported to influence the skin wound healing process by finely regulating autophagy. Biomaterials that regulate autophagy in various cells involved in skin wound healing to regulate the differentiation, proliferation and migration of cells, inflammatory responses, oxidative stress and formation of the extracellular matrix (ECM) have emerged as a key method for improving the tissue regeneration ability of biomaterials. During the inflammatory phase, autophagy enhances the clearance of pathogens from the wound site and leads to macrophage polarization from the M1 to the M2 phenotype, thus preventing enhanced inflammation that can lead to further tissue damage. Autophagy plays important roles in facilitating the formation of extracellular matrix (ECM) during the proliferative phase, removing excess intracellular ROS, and promoting the proliferation and differentiation of endothelial cells, fibroblasts, and keratinocytes. This review summarizes the close association between autophagy and skin wound healing and discusses the role of biomaterial-based autophagy in tissue regeneration. The applications of recent biomaterials designed to target autophagy are highlighted, including polymeric materials, cellular materials, metal nanomaterials, and carbon-based materials. A better understanding of biomaterial-regulated autophagy and skin regeneration and the underlying molecular mechanisms may open new possibilities for promoting skin regeneration. Moreover, this can lay the foundation for the development of more effective therapeutic approaches and novel biomaterials for clinical applications.