SOS2-AFP2 module regulates seed germination by inducing ABI5 degradation in response to salt stress in Arabidopsis.

Soil salinity pose a significant challenge to global agriculture, threatening crop yields and food security. Understanding the salt tolerance mechanisms of plants is crucial for improving their survival under salt stress. AFP2, a negative regulator of ABA signaling, has been shown to play a crucial role in salt stress tolerance during seed germination. Mutations in AFP2 gene lead to increased sensitivity to salt stress. However, the underline mechanisms by which AFP2 regulates seed germination under salt stress remain elusive. In this study, we identified a protein interaction between AFP2 and SOS2, a Ser/Thr protein kinase known to play a critical role in salt stress response. Using a combination of genetic, biochemical, and physiological approaches, we investigated the role of the SOS2-AFP2 module in regulating seed germination under salt stress. Our findings reveal that SOS2 physically interacts with AFP2 and stabilizes it, leading to the degradation of the ABI5 protein, a negative transcription factor in seed germination under salt stress. This study sheds light on previously unknown connections within salt stress and ABA signaling, paving the way for novel strategies to enhance plant resilience against environmental challenges.

Latent profile analysis of empathy ability and its relationship with professional quality of life among hospice nurses in China.

BACKGROUND: Empathy is important in hospice nursing clinics and may influence nurses' professional quality of life (ProQOL). However, present studies ignoring each empathic dimension, and few researches have explored the correlation between empathy and ProQOL in hospice nurses in Asia. To better understand hospice nurses' empathy abilities in China and its relationship with ProQOL, the aim of this study was to identify the latent profiles and its influencing factors of hospice nurses' empathy ability, as well as differences in ProQOL across each latent profile. METHODS: A cross-sectional study was conducted from October 2021 to September 2022, and a total of 725 hospice nurses were recruited from different geographic regions in China. Participants completed the Empathy Ability Scale for Hospice Nurses and the Brief Professional Quality of Life Scale. Latent profile analysis (LPA) was employed to identify latent profiles of empathy ability among hospice nurses in China. The predictors of hospice nurses' empathy ability in different latent profiles were assessed using multinomial logistic regression analysis. One-way ANOVA test and the Kruskal-Wallis test were used to compare the ProQOL scores in each latent profile of nurses' empathy ability. RESULTS: This study identified three latent profiles of hospice nurses' empathy ability, and those profiles labelled "poor empathy ability-high surface empathy expression" (n = 216, 29.8%), "moderate empathy ability" (n = 359, 49.5%) and "high empathy ability-high deep empathy expression" (n = 150, 20.7%). Multinomial logistic regression analysis suggested that age, hospital level, whether income meets expectations, interests in hospice care work, hospice work experience, and receiving psychological counselling were predictors of hospice nurses' profile membership of empathy ability. The scores of compassion satisfaction (CS) and burnout (BO) in ProQOL were significantly different across each profile (P < 0.001), while scores of secondary traumatic stress (STS) in ProQOL were not different across each profile (P = 0.294). CONCLUSIONS: Hospice nurses' empathy ability was divided into three latent profiles, and enhancing empathy ability may be conducive to improving hospice nurses' CS, while reducing BO, thus fostering their overall quality of life. Nursing managers should identify hospice nurses at higher risk of BO and implement targeted interventions focused on enhancing nurse's empathy abilities.

Enantioselective Synthesis of Biscyclopropanes Using Alkynes as Dicarbene Equivalents.

Chiral biscyclopropanes are an important skeleton in many bioactive molecules. However, there are few routes to synthesize these molecules with high stereoselectivity due to the nature of multiple stereocenters. Herein, we report the first example of Rh2 (II)-catalyzed enantioselective synthesis of bicyclopropanes with alkynes as dicarbene equivalents. The bicyclopropanes with 4-5 vicinal stereocenters and 2-3 all-carbon quaternary centers were constructed in excellent stereoselectivity. This protocol features high efficiency and excellent functional group tolerance. Moreover, the protocol was also extended to the cascaded cyclopropanation/cyclopropenation with excellent stereoselectivities. In these processes, both sp-carbons of alkyne were converted into stereogenic sp3 -carbons. Experimental and density functional theory (DFT) calculations revealed that the cooperative weak hydrogen bonds between the substrates and the dirhodium catalyst may play key roles in this reaction.

N6-methyladenosine RNA modification and its interaction with regulatory non-coding RNAs in colorectal cancer.

As one of the most common forms of RNA modification, N6-methyladenosine (m6A) RNA modification has attracted increasing research interest in recent years. This reversible RNA modification added a new dimension to the post-transcriptional regulation of gene expression. In colorectal cancer (CRC), the role of m6A modification has been extensively studied, not only on mRNAs but also on non-coding RNAs (ncRNAs). In the present review, we depicted the role of m6A modification in CRC, systematically elaborate the interaction between m6A modification and regulatory ncRNAs in function and mechanism. Moreover, we discussed the potential applications in clinical.

Dioscin alleviates lipopolysaccharide-induced acute lung injury through suppression of TLR4 signaling pathways.

Aim: Acute lung injury (ALI) is a life-threatening inflammatory syndrome that lacks an effective therapy. Dioscin, a natural steroid saponin isolated from a variety of herbs, could serve as an anti-inflammatory agent, as suggested in previous reports. The purpose of this study was to explore the effects of dioscin on lipopolysaccharide (LPS)-induced ALI and validate the potential mechanisms.Materials and Methods: An ALI model was induced by intratracheal administration of LPS. Dioscin (20, 40, and 80 mg/kg) was administered intragastrically once daily for seven consecutive days prior to LPS challenge.Results: Our data revealed that dioscin significantly suppressed LPS-induced lung pathological changes, pulmonary capillary permeability, pulmonary edema, inflammatory cell infiltration, myeloperoxidase (MPO) activity, and cytokine production, including tumor necrosis factor (TNF)-α, interleukin (IL)-6, and keratinocyte chemoattractant (KC). Moreover, dioscin inhibited LPS-induced nuclear factor-kappaB (NF-κB) activation as well as Toll-like receptor 4 (TLR4) expression.Conclusions: In brief, the results indicated that dioscin alleviates LPS-induced ALI through suppression of TLR4 signaling pathways.

Caspase-1 inhibitor exerts brain-protective effects against sepsis-associated encephalopathy and cognitive impairments in a mouse model of sepsis.

Sepsis-associated encephalopathy (SAE) manifested clinically in acute and long-term cognitive impairments and associated with increased morbidity and mortality worldwide. The potential pathological changes of SAE are complex and remain to be elucidated. Pyroptosis, a novel programmed cell death, is executed by caspase-1-cleaved GSDMD N-terminal (GSDMD-NT) and we investigated it in peripheral blood immunocytes of septic patients previously. Here, a caspase-1 inhibitor VX765 was treated with CLP-induced septic mice. Novel object recognition test indicated that VX765 treatment reversed cognitive dysfunction in septic mice. Elevated plus maze, tail suspension test and open field test revealed that depressive-like behaviors of septic mice were relieved. Inhibited caspase-1 suppressed the expressions of GSDMD and its cleavage form GSDMD-NT, and reduced pyroptosis in brain at day 1 and day 7 after sepsis. Meantime, inhibited caspase-1 mitigated the expressions of IL-1ß, MCP-1 and TNF-α in serum and brain, diminished microglia activation in septic mice, and reduced sepsis-induced brain-blood barrier disruption and ultrastructure damages in brain as well. Inhibited caspase-1 protected the synapse plasticity and preserved long-term potential, which may be the possible mechanism of cognitive functions protective effects of septic mice. In conclusion, caspase-1 inhibition exerts brain-protective effects against SAE and cognitive impairments in a mouse model of sepsis.

AFP2 as the novel regulator breaks high-temperature-induced seeds secondary dormancy through ABI5 and SOM in Arabidopsis thaliana.

Imbibed seeds monitor environmental and endogenous signals to break dormancy and initiate growth under appropriate conditions. In Arabidopsis thaliana, high temperature (HT) induces secondary seed dormancy, but the underlying mechanism remains unclear. In this study, we found that the abi5-1 mutant was insensitive to high temperature, whereas plants overexpressing ABI5 displayed sensitivity. We then identified ABA-insensitive five-binding protein 2 (AFP2), which interacts with ABI5 and is involved in HT-induced secondary seed dormancy. Under HT stress, the loss-of-function afp2 mutant showed lower seeds germination frequency, reversely, AFP2 overexpressing lines (OE-AFP2) showed high germination frequency. Similar to the abi5 mutant, the crossed OE-AFP2 abi5 or afp2 abi5 lines showed high germination under HT, suggesting that ABI5 is epistatic to AFP2. SOM is reported to negatively regulate seeds germination by altering GA/ABA metabolism, here we found that AFP2 and ABI5 altered SOM transcription. Specifically, overexpressing AFP2 suppressed SOM transcription, resulting in high expression of GA biosynthesis-related genes and low expression of ABA biosynthesis-related genes, ultimately promoting seed germination under HT. Thus, our data demonstrate that AFP2 is a novel regulator to control HT-induced secondary seed dormancy through ABI5 and SOM.

Facile synthesis of AuPd nanoparticles anchored on TiO2 nanosheets for efficient dehydrogenation of formic acid.

Safe and efficient hydrogen storage is one of the key technologies for the widespread utilization of hydrogen energy. Formic acid (FA) is regarded as a safe and convenient chemical hydrogen storage material. However, the lack of highly efficient heterogeneous catalysts hinders its practical application. Herein, we presented a facile wet-impregnated deposition method to synthesize ultrafine AuPd alloy nanoparticles anchored on TiO2 nanosheets (AuPd/TiO2 nanosheets) which were used as high efficient catalysts for the dehydrogenation of FA. TiO2 nanosheets were calcined at different temperatures to modify the catalytic activity of catalyst. AuPd/TiO2 nanosheets-400 exhibits the superior activity for catalyzing the FA to release 96% of overall hydrogen content with an initial turnover frequency value of 592 mol H2 mol-1 metal h-1 at 25 °C and low activation energy of 11.8 kJ mol-1. Detailed characterizations show that the superior catalytic performance can be ascribed to the alloy structure of AuPd centers, the phase and crystallinity of TiO2 nanosheets, and the strong electron transfer interaction between AuPd nanoparticles and TiO2 nanosheets substrate.

In situ synthesized SnO2 nanorod/reduced graphene oxide low-dimensional structure for enhanced lithium storage.

A unique SnO2 nanorod (NR)/reduced graphene oxide (RGO) composite morphology has been synthesized using the in situ hydrothermal method, for use as an anode material in lithium-ion batteries. The SnO2 NR adhering to the RGO exhibits a length of 250-400 nm and a diameter of 60-80 nm without any obvious aggregation. The initial discharge/charge capacities of the SnO2 NR/RGO composite are 1761.3 mAh g-1 and 1233.1 mAh g-1, with a coulombic efficiency (CE) of 70% under a current density of 200 mA g-1, and a final capacity of 1101 mAh g-1 after 50 cycles. The rate capability of the SnO2 NR/RGO is also improved compared to that of bare SnO2 NR. The superior electrochemical performance is ascribed to the special morphology of the SnO2 NRs-which plays a role in shorting the transmission path-and the sheet-like 2D graphene, which prevents the agglomeration of SnO2 and enhances conductivity during the electrochemical reaction of SnO2 NR/RGO.

Proteasome-mediated degradation of FRIGIDA modulates flowering time in Arabidopsis during vernalization.

Winter-annual accessions of Arabidopsis thaliana require either exposure to cold stress or vernalization to initiate flowering via FRIGIDA (FRI). FRI acts as a scaffold protein to recruit several chromatin modifiers that epigenetically modify flowering genes. Here, we report that proteasome-mediated FRI degradation regulates flowering during vernalization in Arabidopsis. Our genetic and biochemical experiments demonstrate that FRI directly interacts with the BTB (Bric-a-Brac/Tramtrack/Broad Complex) proteins LIGHT-RESPONSE BTB1 (LRB1) and LRB2 as well as the CULLIN3A (CUL3A) ubiquitin-E3 ligase in vitro and in vivo, leading to proteasomal degradation of FRI during vernalization. The degradation of FRI is accompanied by an increase in the levels of the long noncoding RNA ColdAIR, which reduces the level of histone H3Lys4 trimethylation (H3K4me3) in FLOWERING LOCUS C chromatin to promote flowering. Furthermore, we found that the cold-induced WRKY34 transcription factor binds to the W-box in the promoter region of CUL3A to modulate CUL3A expression. Deficiency of WRKY34 suppressed CUL3A transcription to enhance FRI protein stability and led to late flowering after vernalization. Conversely, overexpression of WRK34 promoted FRI degradation and early flowering through inducing CUL3A accumulation. Together, these data suggest that WRKY34-induced and CUL3A-dependent proteolysis of FRI modulate flowering in response to vernalization.

Association of single nucleotide polymorphisms of APOBEC3G with susceptibility to HIV-1 infection and disease progression among men engaging in homosexual activity in northern China.

Men who have sex with men (MSM) are at high risk of HIV infection. The APOBEC3G (apolipoprotein B mRNA editing catalytic polypeptide 3G) protein is a component of innate antiviral immunity that inhibits HIV-1 replication. In the present study, a total of 483 HIV-1 seropositive men and 493 HIV-1 seronegative men were selected to investigate the association between single nucleotide polymorphisms (SNPs) of the APOBEC3G gene and susceptibility to HIV-1 infection and AIDS progression among MSM residing in northern China. Genotyping of four SNPs (rs5757465, rs3736685, rs8177832, and rs2899313) of the APOBEC3G was performed using the SNPscan™ Kit, while the rs2294367 polymorphism was genotyped using the SNaPshot multiplex system. Our results disclosed no association between the SNPs of APOBEC3G and susceptibility to HIV-1, or effects of these polymorphisms on the CD4+ T cell count or clinical phase of disease. A meta-analysis of 1624 men with HIV-1 infection and 1523 controls suggested that the association between rs8177832 and susceptibility was not significant. However, we observed a trend towards association with HIV-1 infection for haplotype TTACA (p = 0.082). The potential role of variants of APOBEC3G in HIV-1/AIDS warrants further investigation.

Comparative proteomic analysis reveals the role of hydrogen sulfide in the adaptation of the alpine plant Lamiophlomis rotata to altitude gradient in the Northern Tibetan Plateau.

MAIN CONCLUSION: We found the novel role of hydrogen sulfide in the adaptation of the alpine plant to altitude gradient in the Northern Tibetan Plateau. Alpine plants have developed strategies to survive the extremely cold conditions prevailing at high altitudes; however, the mechanism underlying the evolution of these strategies remains unknown. Hydrogen sulfide (H2S) is an essential messenger that enhances plant tolerance to environmental stress; however, its role in alpine plant adaptation to environmental stress has not been reported until now. In this work, we conducted a comparative proteomics analysis to investigate the dynamic patterns of protein expression in Lamiophlomis rotata plants grown at three different altitudes. We identified and annotated 83 differentially expressed proteins. We found that the levels and enzyme activities of proteins involved in H2S biosynthesis markedly increased at higher altitudes, and that H2S accumulation increased. Exogenous H2S application increased antioxidant enzyme activity, which reduced ROS (reactive oxygen species) damage, and GSNOR (S-nitrosoglutathione reductase) activity, which reduced RNS (reactive nitrogen species) damage, and activated the downstream defense response, resulting in protein degradation and proline and sugar accumulation. However, such defense responses could be reversed by applying H2S biosynthesis inhibitors. Based on these findings, we conclude that L. rotata uses multiple strategies to adapt to the alpine stress environment and that H2S plays a central role during this process.

An enhanced informed watermarking scheme using the posterior hidden Markov model.

Designing a practical watermarking scheme with high robustness, feasible imperceptibility, and large capacity remains one of the most important research topics in robust watermarking. This paper presents a posterior hidden Markov model (HMM-) based informed image watermarking scheme, which well enhances the practicability of the prior-HMM-based informed watermarking with favorable robustness, imperceptibility, and capacity. To make the encoder and decoder use the (nearly) identical posterior HMM, each cover image at the encoder and each received image at the decoder are attacked with JPEG compression at an equivalently small quality factor (QF). The attacked images are then employed to estimate HMM parameter sets for both the encoder and decoder, respectively. Numerical simulations show that a small QF of 5 is an optimum setting for practical use. Based on this posterior HMM, we develop an enhanced posterior-HMM-based informed watermarking scheme. Extensive experimental simulations show that the proposed scheme is comparable to its prior counterpart in which the HMM is estimated with the original image, but it avoids the transmission of the prior HMM from the encoder to the decoder. This thus well enhances the practical application of HMM-based informed watermarking systems. Also, it is demonstrated that the proposed scheme has the robustness comparable to the state-of-the-art with significantly reduced computation time.

Self-efficacy as mediators of the association between dyadic coping and quality of life among spousal caregiver of patients with cervical cancer.

Objective: This study aims to explore the influence of dyadic coping (DC) on the quality of life (QoL) of spousal caregivers for patients with cervical cancer and to investigate the mediating role of self-efficacy in this relationship. Methods: A convenience sample of 206 spouses of cervical cancer patients from five hospitals in Jiangsu Province, China, was included in the study. The participants completed three instruments: the 12-item Short-Form Health Survey, the General Self-Efficacy Scale, and the Dyadic Coping Inventory. Structural Equation Modeling (SEM) was used to analyze the mediating effect of self-efficacy in the DC and QoL relationship. Results: The study found a positive correlation between self-efficacy and DC. Self-efficacy partially mediated the impact of DC on QoL, accounting for 16% of the total effect. Self-efficacy played a mediating role in facilitating the indirect positive effects of DC on QoL. Conclusions: Spousal caregivers of cervical cancer patients frequently experience a relatively low QoL. The results suggest that interventions aimed at enhancing DC among spousal caregivers should incorporate strategies to improve self-efficacy, given its mediating role in the positive relationship between DC and QoL.

Dirhodium-Catalyzed Enantioselective Synthesis of Difluoromethylated Cyclopropanes via Enyne Cycloisomerization.

(Difluoromethylated cyclopropane represents an important motif, which is widely found in bioactive and functional molecules. Despite significant progress in modern chemistry, the atom-economic and enantioselective synthesis of difluoromethylated cyclopropanes is still challenging. Herein, an Rh2 (II)-catalyzed asymmetric enyne cycloisomerization is described to construct chiral difluoromethylated cyclopropane derivatives with up to 99% yield and 99% ee in low catalyst loading (0.2 mol%), which can be easily transformed into highly functionalized difluoromethylated cyclopropanes with vicinal all-carbon quaternary stereocenters by ozonolysis. Mechanistic studies and the crystal structures of alkyne-dirhodium complexes reveal that the cooperative weak hydrogen bondings between the substrates and the dirhodium catalyst may play key roles in this reaction.).

PDGFß receptor-targeted delivery of truncated transforming growth factor ß receptor type II for improving the in vitro and in vivo anti-renal fibrosis activity via strong inactivation of TGF-ß1/Smad signaling pathway.

Truncated transforming growth factor ß receptor type II (tTßRII), serving as a trap for binding excessive transforming growth factor ß1 (TGF-ß1) by means of competing with wild-type TßRII, is a promising strategy for the treatment of kidney fibrosis. Platelet-derived growth factor ß receptor (PDGFßR) is highly expressed in interstitial myofibroblasts in kidney fibrosis. This study identified the interaction between a novel tTßRII variant Z-tTßRII (PDGFßR-specific affibody ZPDGFßR fused to the N-terminus of tTßRII) and TGF-ß1. Moreover, Z-tTßRII highly targeted to TGF-ß1-activated NIH3T3 cells and UUO-induced fibrotic kidney, but less to normal cells, tissues, and organs. Furthermore, Z-tTßRII significantly inhibited cell proliferation and migration, and reduced fibrosis markers expression and phosphorylation level of Smad2/3 in activated NIH3T3 cells. Meanwhile, Z-tTßRII markedly alleviated the kidney histopathology and fibrotic responses, and inhibited the TGF-ß1/Smad signaling pathway in UUO mice. Besides, Z-tTßRII showed good safety performance in the treatment of UUO mice. In conclusion, these results demonstrated that Z-tTßRII may be a potential candidate for a targeting therapy on renal fibrosis due to the high potential of fibrotic kidney-targeting and strong anti-renal fibrosis activity.

Identification of ferroptosis-associated genes and potential pharmacological targets in sepsis-induced myopathy.

Background: The role of Ferroptosis in the course of sepsis-induced myopathy is yet unclear. The objective of our work is to identify key genes connected with Ferroptosis in sepsis-induced myopathy and investigate possible pharmaceutical targets related to this process. This research aims to provide new insights into the management of sepsis-induced myopathy. Methods: We got the GSE13205 dataset from the Gene Expression Omnibus (GEO) and extracted Ferroptosis-associated genes from the FerrDb database. After conducting a functional annotation analysis of these genes, we created a protein-protein interaction network using Cytoscape software to identify important genes. Subsequently, we employed CMap to investigate prospective pharmaceuticals that could target these crucial genes. Results: A total of 61 genes that are expressed differently (DEGs) have been found concerning Ferroptosis. These genes are involved in a wide range of biological functions, including reacting to signals from outside the cell and the availability of nutrients, programmed cell death, controlling apoptosis, and responding to peptides, chemical stressors, and hormones. The KEGG pathway study revealed that these pathways are involved in Ferroptosis, autophagy, P53 signaling, PI3K-Akt signaling, mTOR signaling, HIF-1 signaling, endocrine resistance, and different tumorigenic processes. In addition, we created a network that shows the simultaneous expression of important genes and determined the top 10 medications that have the potential to treat sepsis-induced myopathy. Conclusion: The bioinformatics research undertaken sheds insight into the probable role of Ferroptosis-associated genes in sepsis-induced myopathy. The identified critical genes show potential as therapeutic targets for treating sepsis-induced myopathy, offering opportunities for the development of tailored medicines.

Gene Mutations in Gastrointestinal Stromal Tumors: Advances in Treatment and Mechanism Research.

Although gastrointestinal stromal tumors (GISTs) has been reported in patients of all ages, its diagnosis is more common in elders. The two most common types of mutation, receptor tyrosine kinase (KIT) and platelet-derived growth factor receptor a (PDGFRA) mutations, hold about 75 and 15% of GISTs cases, respectively. Tumors without KIT or PDGFRA mutations are known as wild type (WT)-GISTs, which takes up for 15% of all cases. WT-GISTs have other genetic alterations, including mutations of the succinate dehydrogenase and serine-threonine protein kinase BRAF and neurofibromatosis type 1. Other GISTs without any of the above genetic mutations are named "quadruple WT" GISTs. More types of rare mutations are being reported. These mutations or gene fusions were initially thought to be mutually exclusive in primary GISTs, but recently it has been reported that some of these rare mutations coexist with KIT or PDGFRA mutations. The treatment and management differ according to molecular subtypes of GISTs. Especially for patients with late-stage tumors, developing a personalized chemotherapy regimen based on mutation status is of great help to improve patient survival and quality of life. At present, imatinib mesylate is an effective first-line drug for the treatment of unresectable or metastatic recurrent GISTs, but how to overcome drug resistance is still an important clinical problem. The effectiveness of other drugs is being further evaluated. The progress in the study of relevant mechanisms also provides the possibility to develop new targets or new drugs.

GSDMD knockout alleviates sepsis-associated skeletal muscle atrophy by inhibiting IL18/AMPK signaling.

BACKGROUND: Sepsis commonly leads to skeletal muscle atrophy, characterized by substantial muscle weakness and degeneration, ultimately contributing to an adverse prognosis. Studies have shown that programmed cell death is an important factor in the progression of muscle loss in sepsis. However, the precise role and mechanism of pyroptosis in skeletal muscle atrophy are not yet fully comprehended. Therefore, we aimed to examine the role and mechanism of action of the pyroptosis effector protein GSDMD in recognized cellular and mouse models of sepsis. METHODS: The levels of GSDMD and N-GSDMD in skeletal muscle were evaluated 2, 4, and 8 days after CLP. Sepsis was produced in mice that lacked the Gsdmd gene (Gsdmd knockout) and in mice with the normal Gsdmd gene (wild-type) using a procedure called cecal ligation and puncture (CLP). The degree of muscular atrophy in the gastrocnemius and tibialis anterior muscles was assessed 72 hours after surgery in the septic mouse model. In addition, the architecture of skeletal muscles, protein expression, and markers associated with pathways leading to muscle atrophy were examined in mice from various groups 72 hours after surgery. The in vitro investigations entailed the use of siRNA to suppress Gsdmd expression in C2C12 cells, followed by stimulation of these cells with lipopolysaccharide (LPS) to evaluate the impact of Gsdmd downregulation on muscle atrophy and the related signaling cascades. RESULTS: This study has demonstrated that the GSDMD protein, known as the "executive" protein of pyroptosis, plays a crucial role in the advancement of skeletal muscle atrophy in septic mice. The expression of N-GSDMD in the skeletal muscle of septic mice was markedly higher compared to the control group. The Gsdmd knockout mice exhibited notable enhancements in survival, muscle strength, and body weight compared to the septic mice. Deletion of the Gsdmd gene reduced muscular wasting in the gastrocnemius and tibialis anterior muscles caused by sepsis. Studies conducted in living organisms (in vivo) and in laboratory conditions (in vitro) have shown that the absence of the Gsdmd gene decreases indicators of muscle loss associated with sepsis by blocking the IL18/AMPK signaling pathway. CONCLUSION: The results of this study demonstrate that the lack of Gsdmd has a beneficial effect on septic skeletal muscle atrophy by reducing the activation of IL18/AMPK and inhibiting the UPS and autophagy pathways. Therefore, our research provides vital insights into the role of pyroptosis in sepsis-related skeletal muscle wasting, which could potentially lead to the development of therapeutic and interventional approaches for preventing septic skeletal muscle atrophy.

Role of mesenchymal stem cells in sepsis and their therapeutic potential in sepsis­associated myopathy (Review).

Sepsis­induced myopathy (SIM) is one of the leading causes of death in critically ill patients. SIM mainly involves the respiratory and skeletal muscles of patients, resulting in an increased risk of lung infection, aggravated respiratory failure, and prolonged mechanical ventilation and hospital stay. SIM is also an independent risk factor associated with increased mortality in critically ill patients. At present, no effective treatment for SIM has yet been established. However, mesenchymal stem cells (MSCs) have emerged as a promising therapeutic approach and have been utilized in the treatment of various clinical conditions. A significant body of basic and clinical research supports the efficacy of MSCs in managing sepsis and muscle­related diseases. This literature review aims to explore the relationship between MSCs and sepsis, as well as their impact on skeletal muscle­associated diseases. Additionally, the present review discusses the potential mechanisms and therapeutic benefits of MSCs in the context of SIM.