Drp1 acetylation mediated by CDK5-AMPK-GCN5L1 axis promotes cerebral ischemic injury via facilitating mitochondrial fission.

The aberrant acetylation of mitochondrial proteins is involved in the pathogenesis of multiple diseases including neurodegenerative diseases and cerebral ischemic injury. Previous studies have shown that depletion of mitochondrial NAD+, which is necessary for mitochondrial deacetylase activity, leads to decreased activity of mitochondrial deacetylase and thus causes hyperacetylation of mitochondrial proteins in ischemic brain tissues, which results in altered mitochondrial dynamics. However, it remains largely unknown about how mitochondrial dynamics-related protein Drp1 is acetylated in ischemic neuronal cells and brain tissues. Here, we showed that Drp1 and GCN5L1 expression was up-regulated in OGD-treated neuronal cells and ischemic brain tissues induced by dMCAO, accompanied by the increased mitochondrial fission, mtROS accumulation, and cell apoptosis. Further, we confirmed that ischemia/hypoxia promoted Drp1 interaction with GCN5L1 in neuronal cells and brain tissues. GCN5L1 knockdown attenuated, while its overexpression enhanced Drp1 acetylation and mitochondrial fission, indicating that GCN5L1 plays a crucial role in ischemia/hypoxia-induced mitochondrial fission by acetylating Drp1. Mechanistically, ischemia/hypoxia induced Drp1 phosphorylation by CDK5 upregulation-mediated activation of AMPK in neuronal cells, which in turn facilitated the interaction of GCN5L1 with Drp1, thus enhancing Drp1 acetylation and mitochondrial fission. Accordingly, inhibition of AMPK alleviated ischemia/hypoxia- induced Drp1 acetylation and mitochondrial fission and protected brain tissues from ischemic damage. These findings provide a novel insight into the functional roles of GCN5L1 in regulating Drp1 acetylation and identify a previously unrecognized CDK5-AMPK-GCN5L1 pathway that mediates the acetylation of Drp1 in ischemic brain tissues.

ROS-mediated up-regulation of SAE1 by Helicobacter pylori promotes human gastric tumor genesis and progression.

Helicobacter pylori (H. pylori) is a major risk factor of gastric cancer (GC). The SUMO-activating enzyme SAE1(SUMO-activating enzyme subunit 1), which is indispensable for protein SUMOylation, involves in human tumorigenesis. In this study, we used the TIMER and TCGA database to explore the SAE1 expression in GC and normal tissues and Kaplan-Meier Plotter platform for survival analysis of GC patients. GC tissue microarray and gastric samples from patients who underwent endoscopic treatment were employed to detect the SAE1expression. Our results showed that SAE1 was overexpressed in GC tissues and higher SAE1 expression was associated with worse clinical characteristics of GC patients. Cell and animal models showed that H. pylori infection upregulated SAE1, SUMO1, and SUMO2/3 protein expression. Functional assays suggested that suppression of SAE1 attenuated epithelial-mesenchymal transition (EMT) biomarkers and cell proliferation abilities induced by H. pylori. Cell and animal models of ROS inhibition in H. pylori showed that ROS could mediate the H. pylori-induced upregulation of SAE1, SUMO1, and SUMO2/3 protein. RNA sequencing was performed and suggested that knockdown of SAE1 could exert an impact on IGF-1 expression. General, increased SUMOylation modification is involved in H. pylori-induced GC.

Vascular endothelial glycocalyx shedding in ventilator-induced lung injury in rats.

Endothelial permeability deterioration is involved in ventilator-induced lung injury (VILI). The integrality of vascular endothelial glycocalyx (EG) is closely associated with endothelial permeability. The hypothesis was that vascular EG shedding participates in VILI through promoting endothelial permeability. In the present study, male Sprague-Dawley (SD) rats were ventilated with high tidal volume (VT =40 ml/kg) or low tidal volume (VT =8 ml/kg) to investigate the effects of different tidal volume and ventilation durations on EG in vivo. We report disruption of EG during the period of high tidal volume ventilation characterized by increased glycocalyx structural components (such as syndecan-1, heparan sulfate, hyaluronan) in the plasma and decreased the expression of syndecan-1 in the lung tissues. Mechanistically, the disruption of EG was associated with increased proinflammatory cytokines and matrix metalloproteinase in the lung tissues. Collectively, these results demonstrate that the degradation of EG is involved in the occurrence and development of VILI in rats, and the inflammatory mechanism mediated by activation of the NF-κB signaling pathway may be partly responsible for the degradation of EG in VILI in rats. This study enhances our understanding of the pathophysiological processes underlying VILI, shedding light on potential therapeutic targets to mitigate VILI.

Exploration of mitochondrial autophagy related genes in the diagnosis model construction and molecular marker mining of Alzheimer's disease based on multi-omics integration.

Key features of Alzheimer's disease include neuronal loss, accumulation of beta-amyloid plaques, and formation of neurofibrillary tangles. These changes are due in part to abnormal protein metabolism, particularly the accumulation of amyloid beta. Mitochondria are the energy production centers within cells and are also the main source of oxidative stress. In AD, mitochondrial function is impaired, leading to increased oxidative stress and the production of more reactive oxidative substances, further damaging cells. Mitophagy is an important mechanism for maintaining mitochondrial health, helping to clear damaged mitochondria, prevent the spread of oxidative stress, and reduce abnormal protein aggregation. To this end, this article conducts an integrated analysis based on DNA methylation and transcriptome data of AD. After taking the intersection of the genes where the differential methylation sites are located and the differential genes, machine learning methods were used to build an AD diagnostic model. This article screened five diagnostic genes ATG12, CSNK2A2, CSNK2B, MFN1 and PGAM5 and conducted experimental verification. The diagnostic genes discovered and the diagnostic model constructed in this article can provide reference for the development of clinical diagnostic models for AD.

Is the interspinous process device safe and effective in elderly patients with lumbar degeneration? A systematic review and meta-analysis of randomized controlled trials.

BACKGROUND CONTEXT: Lumbar spinal stenosis is one of the most common diseases affecting the elderly that is characterized by the narrowing of the spinal canal and peripheral neural pathways which may cause back pain and neurogenic intermittent claudication in affected patients. Recently, as an alternative treatment between conservative therapy and decompression surgery, interspinous process device (IPD) such as X-stop, Coflex, DIAM, Aperius, Wallis, etc., has gained enough popularity. PURPOSE: The purpose of this study was to evaluate the efficacy and safety of IPD in the treatment of degenerative lumbar spinal stenosis compared with decompression surgery. STUDY DESIGN: This study was a systematic review and meta-analysis of randomized controlled trials. PATIENT SAMPLE: 555 patients' samples were collected for this study. OUTCOME MEASURES: The Visual Analogue Scale and the Oswestry Disability Index were analyzed, as well as the Zurich Claudication Questionnaire For efficacy evaluation. Complication and reoperation rate was utilized for the assessment of safety. METHODS: A comprehensive literature search was performed through Pubmed, EMBASE, Web of Science, and Cochrane Library until October 2023. Among the studies meeting the eligible criteria, any study in which IPD was utilized in the treatment of degenerative lumbar spinal stenosis was included in the current review. For efficacy evaluation, the Visual Analogue Scale and the Oswestry Disability Index were analyzed, as well as the Zurich Claudication Questionnaire. Complication and reoperation rates were utilized for the assessment of safety. RESULTS: Five randomized controlled trials with 555 patients were included. There were no significant differences in VAS leg pain (SMD - 0.08, 95% CI - 0.32 to 0.15) and back pain (SMD 0.09, 95%CI-0.27 to 0.45), ODI scores (MD 1.08, 95% CI - 11.23 to 13.39) and ZCQ physical function (MD-0.09, 95% CI-0.22 to 0.05) for IPD compared with decompression surgery. In terms of ZCQ symptom severity (MD - 0.22, 95% CI - 0.27 to - 016), decompression surgery showed superior to the IPD. As for complications (RR 1.08, 95% CI 0.36 to 3.27), the IPD had no advantages compared to decompression surgery, whereas inferior to it in reoperation rate (RR 2.58, 95% CI 1.67 to 3.96). CONCLUSIONS: This systematic review and meta-analysis indicated no superiority in the clinical outcome for IPD compared with decompression surgery. However, more clinical studies are warranted to determine the efficacy and safety of IPD.

Identification of a highly promiscuous glucosyltransferase from Penstemon barbatus for natural product glycodiversification.

Glycosylation reactions mediated by UDP-glycosyltransferases (UGTs) are common post-modifications involved in plant secondary metabolism and significantly improve the solubility and bioactivity of aglycones. Penstemon barbatus is rich in phenylethanoid glycosides (PhGs), such as echinacoside and verbascoside. In this study, a promiscuous glycosyltransferase UGT84A95 was identified from P. barbatus. In vitro enzyme assays showed that UGT84A95 catalyzed the glucosylation of the phenol hydroxyl group of PhGs efficiently as well as other structurally diverse phenolic glycosides, including flavonoids, terpenoids, stilbene glycosides, coumarins, and simple polyphenols. By using UGT84A95, 12 glycosylated products were prepared and structurally identified by NMR spectroscopy, among which 7 are new compounds. These findings suggest that UGT84A95 could be a potential biocatalyst to synthesize multi-glycosylated glycosides.

Effect of perioperative goal-directed fluid therapy on postoperative complications after thoracic surgery with one-lung ventilation: a systematic review and meta-analysis.

BACKGROUND: An understanding of the impact of goal-directed fluid therapy (GDFT) on the outcomes of patients undergoing one-lung ventilation (OLV) for thoracic surgery remains incomplete and controversial. This meta-analysis aimed to assess the effect of GDFT compared to other fluid therapy strategies on the incidence of postoperative complications in patients with OLV. METHODS: The Embase, Cochrane Library, Web of Science, and MEDLINE via PubMed databases were searched from their inception to November 30, 2022. Forest plots were constructed to present the results of the meta-analysis. The quality of the included studies was evaluated using the Cochrane Collaboration tool and Risk Of Bias In Non-Randomized Study of Interventions (ROBINS-I). The primary outcome was the incidence of postoperative complications. Secondary outcomes were the length of hospital stay, PaO2/FiO2 ratio, total fluid infusion, inflammatory factors (TNF-α, IL-6), and postoperative bowel function recovery time. RESULTS: A total of 1318 patients from 11 studies were included in this review. The GDFT group had a lower incidence of postoperative complications [odds ratio (OR), 0.47; 95% confidence interval (95% CI), 0.29-0.75; P = 0.002; I 2, 67%], postoperative pulmonary complications (OR 0.48, 95% CI 0.27-0.83; P = 0.009), and postoperative anastomotic leakage (OR 0.51, 95% CI 0.27-0.97; P = 0.04). The GDFT strategy reduces total fluid infusion. CONCLUSIONS: GDFT is associated with lower postoperative complications and better survival outcomes after thoracic surgery for OLV.

Peri-procedural variables and outcomes of long-period hemodynamic instability after carotid artery angioplasty and stenting.

OBJECTIVES: The aim of this study is to identify the peri-procedural risk factors and outcomes of hemodynamic instability (HI) after carotid artery stenting (CAS). METHODS: A single-center, retrospective study was performed in 168 patients who underwent CAS procedure between September 2017 and September 2020. The presence of HI, as defined by hypertension (systolic blood pressure >160 mmHg), hypotension (systolic blood pressure <90 mmHg), and/or bradycardia (heart rate <60 bpm), was recorded. Long-period HI was defined as persistent HI lasting more than 24 h. Patient demographics, comorbidities, peri-procedural variables, and risk factors were recorded. Clinical outcomes including cerebral hyperperfusion syndrome, hemorrhage, transient ischemic attack (TIA), stroke, myocardial infarction, and mortality within 30 days of the procedure were evaluated. Logistic regression was used to analyze the independent risk factors of long-period HI following CAS. RESULTS: Among 168 patients (mean age, 68.2 ± 8.3 years; 81.5% male), the frequency of post-procedural long-period HI was noted in 42 patients (25.0%). Male was prone to experience HI (odds ratio, 9.156, p = 0.021). Aggressive inflation pressure (>7 atm) and 5 mm balloon for pre-dilatation were risk factors of long-period HI (OR, 7.372, p = 0.035; OR, 3.527, p = 0.023). Intraoperative peak blood pressure and larger-sized stents remained independent predictors for the development of HI (OR, 1.043, p = 0.027, and OR, 1.973, p = 0.015). Patients with prolonged HI were more likely to suffer TIA and stroke compared to other patients and significant difference was found in the occurrence of TIA (p < 0.05). Non-significance was found in mortality rate and other outcomes. CONCLUSIONS: CAS-induced HI occurs in a considerable percentage while several peri-procedural variables are determined as independent predictors to develop long-period HI. Patients with prolonged HI are associated with increased risk of neurologic events and thus standardized intervention as well as management of long-period HI are of critical importance during clinical process.

Chief resident behaviors that lead to effective morning reports, a multisite qualitative study.

BACKGROUND: Morning report is a fundamental component of internal medicine training and often represents the most significant teaching responsibility of Chief Residents. We sought to define Chief Resident behaviors essential to leading a successful morning report. METHODS: In 2016, we conducted a multi-site qualitative study using key informant interviews of morning report stakeholders. 49 residents, Chief Residents, and faculty from 4 Internal Medicine programs participated. Interviews were analyzed and coded by 3 authors using inductive reasoning and thematic analysis. A preliminary code structure was developed and expanded in an iterative process concurrent with data collection until thematic sufficiency was reached and a final structure was established. This final structure was used to recode all transcripts. RESULTS: We identified four themes of Chief Resident behaviors that lead to a successful morning report: report preparation, delivery skills, pedagogical approaches, and faculty participation. Preparation domains include thoughtful case selection, learning objective development, content editing, and report organization. Delivery domains include effective presentation skills, appropriate utilization of technology, and time management. Pedagogical approach domains include learner facilitation techniques that encourage clinical reasoning while nurturing a safe learning environment, as well as innovative teaching strategies. Moderating the involvement of faculty was identified as the final key to morning report effectiveness. Specific behavior examples are provided. CONCLUSION: Consideration of content preparation, delivery, pedagogical approaches, and moderation of faculty participation are key components to Chief Resident-led morning reports. Results from this study could be used to enhance faculty development for Chief Residents.

The sprT Gene of Bacillus velezensis FZB42 Is Involved in Biofilm Formation and Bacilysin Production.

Bacillus velezensis FZB42, a representative strain of plant-growth-promoting rhizobacteria (PGPR), can form robust biofilm and produce multiple antibiotics against a wild range of phytopathogens. In this study, we observed different biofilm morphology of the mutant Y4, derived from a TnYLB-1 transposon insertion library of B. velezensis FZB42. We identified that the transposon was inserted into the sprT gene in Y4. Our bioinformatics analysis revealed that the SprT protein is an unstable hydrophilic protein located in the cytoplasm. It is highly conserved in Bacillus species and predicted to function as a metalloprotease by binding zinc ions. We also demonstrated that ΔsprT significantly reduced the swarming ability of FZB42 by ~5-fold and sporulation capacity by ~25-fold. In addition, the antagonistic experiments showed that, compared to the wild type, the ΔsprT strain exhibited significantly reduced inhibition against Staphylococcus aureus ATCC-9144 and Phytophthora sojae, indicating that the inactivation of sprT led to decreased production of the antibiotic bacilysin. The HPLC-MS analysis confirmed that bacilysin was indeed decreased in the ΔsprT strain, and qPCR analysis revealed that ΔsprT down-regulated the expression of the genes for bacilysin biosynthesis. Our results suggest that the sprT gene plays a regulatory role in multiple characteristics of B. velezensis FZB42, including biofilm formation, swarming, sporulation, and antibiotic production.

A Covalent Organic Framework as a Long-life and High-Rate Anode Suitable for Both Aqueous Acidic and Alkaline Batteries.

Aqueous rechargeable batteries are prospective candidates for large-scale grid energy storage. However, traditional anode materials applied lack acid-alkali co-tolerance. Herein, we report a covalent organic framework containing pyrazine (C=N) and phenylimino (-NH-) groups (HPP-COF) as a long-cycle and high-rate anode for both acidic and alkaline batteries. The HPP-COF's robust covalent linkage and the hydrogen bond network between -NH- and water molecules collectively improve the acid-alkaline co-tolerance. More importantly, the hydrogen bond network promotes the rapid transport of H+ /OH- by the Grotthuss mechanism. As a result, the HPP-COF delivers a superior capacity and cycle stability (66.6 mAh g-1 @ 30 A g-1 , over 40000 cycles in 1 M H2 SO4 electrolyte; 91.7 mAh g-1 @ 100 A g-1 , over 30000 cycles @ 30 A g-1 in 1 M NaOH electrolyte). The work opens a new direction for the structural design and application of COF materials in acidic and alkaline batteries.

Immunogenic cell death and its therapeutic or prognostic potential in high-grade glioma.

Immunogenic cell death (ICD) has emerged as a key component of therapy-induced anti-tumor immunity. Over the past few years, ICD was found to play a pivotal role in a wide variety of novel and existing treatment modalities. The clinical application of these techniques in cancer treatment is still in its infancy. Glioblastoma (GBM) is the most lethal primary brain tumor with a dismal prognosis despite maximal therapy. The development of new therapies in this aggressive type of tumors remains highly challenging partially due to the cold tumor immune environment. GBM could therefore benefit from ICD-based therapies stimulating the anti-tumor immune response. In what follows, we will describe the mechanisms behind ICD and the ICD-based (pre)clinical advances in anticancer therapies focusing on GBM.

The Protective Role of 4-Acetylarylquinolinol B in Different Pathological Processes.

Antrodia cinnamomea is a traditional plant and a unique fungus native to Taiwan that has been reported to have many biological functions, including anti-inflammatory and anticancer activities. The compound 4-acetylarylquinolinol B (4-AAQB) is one of the main bioactive compounds in the stamens of Antrodia cinnamomea, and has many biological functions, such as anti-inflammatory, antiproliferative, blood sugar reduction, antimetastasis, and vascular tone relaxation. In recent years, the increasing evidences have shown that 4-AAQB is involved in many diseases; however, the relevant mechanisms have not been fully clarified. This review aimed to clarify the improvement by 4-AAQB in different pathological processes, as well as the compound's molecular mechanisms, in order to provide a theoretical reference for future related research.

Effect of Electroacupuncture on Short-Chain Fatty Acids in Peripheral Blood after Middle Cerebral Artery Occlusion/Reperfusion in Rats Based on Gas Chromatography-Mass Spectrometry.

Previous fundamental and clinical research has shown that electroacupuncture (EA) at the acupoints of Quchi (LI11) and Zusanli (ST36) can successfully alleviate motor dysfunction following stroke. Additionally, it has been discovered that gut microbiota and their metabolites play an essential role in stroke. However, the relationship between the metabolites of gut microbiota and the efficacy of EA is still unclear. Therefore, the aim of this study was to evaluate the mechanism of EA at LI11 and ST36 in the treatment of motor dysfunction after middle cerebral artery occlusion/reperfusion (MCAO/R) in model rats by comparing the differences and correlation between different short-chain fatty acids (SCFAs) and the recovery of motor function. The results indicated that EA at LI11 and ST36 acupoints enhanced the neurological function, motor function, and infarct volume of MCAO/R rats. The levels of acetic acid, propionic acid, and total SCFAs were considerably lower in the MCAO/R group than in the sham group (P < 0.05). Acetic acid, propionic acid, and total SCFA concentrations were substantially higher in the MCAO/R + EA group than in the MCAO/R group (P < 0.05). Finally, Pearson correlation analysis revealed that the propionic acid concentration was substantially favorably connected with the duration on the rotarod (r = 0.633 and P < 0.05) and highly negatively correlated with the modified neurological severity score (mNSS) (r = -0.698 and P < 0.05) and the percentage of cerebral infarct volume (r = -0.729 and P < 0.05). Taken together, these findings indicate that the increase in propionic acid may be one of the mechanisms and targets of EA at LI11 and ST36 acupoints to improve poststroke motor dysfunction in MCAO/R rats.

Structure and impact of longitudinal Graduate Medical Education curricula designed to prepare future clinician-educators: A systematic scoping review: BEME Guide No. 74.

BACKGROUND: Many Graduate Medical Education (GME) programs offer clinician-educator curricula. The specific instructional methods employed and current best practices for clinician-educator curricula are unknown. We aimed to characterize the structure, curriculum content, instructional methods, and outcomes of longitudinal GME clinician-educator curricula. METHODS: We conducted a scoping review, registered with BEME, by comprehensively searching health science databases and related grey literature from January 2008 to January 2021 for studies involving longitudinal GME curricula aimed to train future clinician-educators. RESULTS: From 9437 articles, 36 unique curricula were included in our review. Most curricula were designed for residents (n = 26) but were heterogeneous in structure, instructional methods, and content. Several curricular themes emerged, including: 1) duration ≥ 12 months, 2) application of theory-based didactics with experiential activities, 3) independent projects, 4) exposure to faculty mentorship and educator communities, 5) strengthening competencies beyond teaching and scholarship, and 6) protected time and funding. Most outcomes were positive and focused on learner satisfaction or behavior change related to scholarly output and career tracking. CONCLUSIONS: Curricula in our review included important skills including experiential teaching, scholarly projects, and exposure to educator communities. Future curricula should build on these competencies and include more assessment of learner and program outcomes.

The Emerging Role of EVA1A in Different Types of Cancers.

Eva-1 homolog A (EVA1A), also known as transmembrane protein 166 (TMEM166) and regulator of programmed cell death, is an endoplasmic reticulum associated protein, which can play an important role in many diseases, including a variety of cancers, by regulating autophagy/apoptosis. However, the related mechanism, especially the role of EVA1A in cancers, has not been fully understood. In this review, we summarize the recent studies on the role of EVA1A in different types of cancers, including breast cancer, papillary thyroid cancer, non-small cell lung cancer, hepatocellular carcinoma, glioblastoma and pancreatic cancer, and analyze the relevant mechanisms to provide a theoretical basis for future related research.

The Role of Autophagy and Pyroptosis in Liver Disorders.

Pyroptosis is a programmed cell death caused by inflammasomes, which can detect cell cytosolic contamination or disturbance. In pyroptosis, caspase-1 or caspase-11/4/5 is activated, cleaving gasdermin D to separate its N-terminal pore-forming domain (PFD). The oligomerization of PFD forms macropores in the membrane, resulting in swelling and membrane rupture. According to the different mechanisms, pyroptosis can be divided into three types: canonical pathway-mediated pyroptosis, non-canonical pathway-mediated pyroptosis, and caspase-3-induced pyroptosis. Pyroptosis has been reported to play an important role in many tissues and organs, including the liver. Autophagy is a highly conserved process of the eukaryotic cell cycle. It plays an important role in cell survival and maintenance by degrading organelles, proteins and macromolecules in the cytoplasm. Therefore, the dysfunction of this process is involved in a variety of pathological processes. In recent years, autophagy and pyroptosis and their interactions have been proven to play an important role in various physiological and pathological processes, and have gradually attracted more and more attention to become a research hotspot. Therefore, this review summarized the role of autophagy and pyroptosis in liver disorders, and analyzed the related mechanism to provide a basis for future research.

The Role of H2S Regulating NLRP3 Inflammasome in Diabetes.

Nucleotide-binding oligomeric domain (NOD)-like receptor protein 3 (NLRP3) is a recently discovered cytoplasmic multiprotein complex involved in inflammation. The NLRP3 inflammasome contains NLRP3, apoptosis-related specific protein (ASC) and precursor caspase-1. The NLRP3 inflammasome is involved in many diseases, including diabetes. H2S is a harmful gas with a rotten egg smell. Recently, it has been identified as the third gas signal molecule after nitric oxide and carbon monoxide. It has many biological functions and plays an important role in many diseases, including diabetes. In recent years, it has been reported that H2S regulation of the NLRP3 inflammasome contributes to a variety of diseases. However, the mechanism has not been fully understood. In this review, we summarized the recent role and mechanism of H2S in regulating the NLRP3 inflammasome in diabetes, in order to provide a theoretical basis for future research.

Hydrogen Sulfide Plays an Important Role by Regulating Endoplasmic Reticulum Stress in Diabetes-Related Diseases.

Endoplasmic reticulum (ER) plays important roles in protein synthesis, protein folding and modification, lipid biosynthesis, calcium storage, and detoxification. ER homeostasis is destroyed by physiological and pharmacological stressors, resulting in the accumulation of misfolded proteins, which causes ER stress. More and more studies have shown that ER stress contributes to the pathogenesis of many diseases, such as diabetes, inflammation, neurodegenerative diseases, cancer, and autoimmune diseases. As a toxic gas, H2S has, in recent years, been considered the third most important gas signal molecule after NO and CO. H2S has been found to have many important physiological functions and to play an important role in many pathological and physiological processes. Recent evidence shows that H2S improves the body's defenses to many diseases, including diabetes, by regulating ER stress, but its mechanism has not yet been fully understood. We therefore reviewed recent studies of the role of H2S in improving diabetes-related diseases by regulating ER stress and carefully analyzed its mechanism in order to provide a theoretical reference for future research.

The Role of Hydrogen Sulfide Regulation of Autophagy in Liver Disorders.

Autophagy is a complex process of degradation of senescent or dysfunctional organelles in cells. Dysfunctional autophagy is associated with many diseases such as cancers, immune dysfunction, and aging. Hydrogen sulfide (H2S) is considered to be the third gas signal molecule after nitrous oxide and carbon monoxide. In recent years, H2S has been found to have a variety of important biological functions, and plays an important role in a variety of physiological and pathological processes. In this review, we review the recent role and mechanism of H2S in regulating autophagy in liver disorders, in order to provide a basis for further research in the future.