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MicroRNAs (miRNAs) are the short endogenous non-coding RNAs that regulate the expression of the target gene at posttranscriptional level through degrading or inhibiting the specific target messenger RNAs (mRNAs). MiRNAs regulate the expression of approximately one-third of protein coding genes, and in most cases inhibit gene expression. MiRNAs have been reported to regulate various biological processes, such as cell proliferation, apoptosis and differentiation. Therefore, miRNAs participate in multiple diseases, including ischemia-reperfusion (I/R) injury. Hydrogen sulfide (H 2 S) was once considered as a colorless, toxic and harmful gas with foul smelling. However, in recent years, it has been discovered that it is the third gas signaling molecule after carbon monoxide (CO) and nitric oxide (NO), with multiple important biological functions. Increasing evidence indicates that H 2 S plays a vital role in I/R injury through regulating miRNA, however, the mechanism has not been fully understood. In this review, we summarized the current knowledge about the role of H 2 S in I/R injury by regulating miRNAs, and analyzed its mechanism in detail., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier Inc.)

Ferroptosis is a programmed cell death that relies on iron and lipid peroxidation. It differs from other forms of programmed cell death such as necrosis, apoptosis and autophagy. More and more evidence indicates that ferroptosis participates in many types of diseases, such as neurodegenerative diseases, ischemia-reperfusion injury, cardiovascular diseases and so on. Hence, clarifying the role and mechanism of ferroptosis in diseases is of great significance for further understanding the pathogenesis and treatment of some diseases. Hydrogen sulfide (H 2 S) is a colorless and flammable gas with the smell of rotten eggs. Many years ago, H 2 S was considered as a toxic gas. however, in recent years, increasing evidence indicates that it is the third important gas signaling molecule after nitric oxide and carbon monoxide. H 2 S has various physiological and pathological functions such as antioxidant stress, anti-inflammatory, anti-apoptotic and anti-tumor, and can participate in various diseases. It has been reported that H 2 S regulation of ferroptosis plays an important role in many types of diseases, however, the related mechanisms are not fully clear. In this review, we reviewed the recent literature about the role of H 2 S regulation of ferroptosis in diseases, and analyzed the relevant mechanisms, hoping to provide references for future in-depth researches., (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Pyroptosis is one kind of programmed cell death in which the cell membrane ruptures and subsequently releases cell contents and pro-inflammatory cytokines including IL-1β and IL-18. Pyroptosis is caused by many types of pathological stimuli, such as hyperglycemia (HG), oxidative stress, and inflammation, and is mediated by gasdermin (GSDM) protein family. Increasing evidence indicates that pyroptosis plays an important role in multiple diseases, such as cancer, kidney diseases, inflammatory diseases, and cardiovascular diseases. Therefore, the regulation of pyroptosis is crucial for the occurrence, development, and treatment of many diseases. Hydrogen sulfide (H 2 S) is a biologically active gasotransmitter following carbon monoxide (CO) and nitrogen oxide (NO) in mammalian tissues. So far, three enzymes, including 3-mercaptopyruvate sulphurtransferase (3-MST), cystathionine γ- Lyase (CSE), and Cystine β-synthesis enzyme (CBS), have been found to catalyze the production of endogenous H 2 S in mammals. H 2 S has been reported to have multiple biological functions including anti-inflammation, anti-oxidative stress, anti-apoptosis and so on. Hence, H 2 S is involved in various physiological and pathological processes. In recent years, many studies have demonstrated that H 2 S plays a critical role by regulating pyroptosis in various pathological processes, such as ischemia-reperfusion injury, alcoholic liver disease, and diabetes cardiomyopathy. However, the relevant mechanism has not been completely understood. Therefore, elucidating the mechanism by which H 2 S regulates pyroptosis in diseases will help understand the pathogenesis of multiple diseases and provide important new avenues for the treatment of many diseases. Here, we reviewed the progress of H 2 S regulation of pyroptosis in different pathological processes, and analyzed the molecular mechanism in detail to provide a theoretical reference for future related research., Competing Interests: Declaration of competing interest The authors declare that there are no conflicts of interest of a financial or personal nature., (Copyright © 2024 Elsevier Masson SAS. All rights reserved.)

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, H 2 S has, in recent years, been considered the third most important gas signal molecule after NO and CO. H 2 S 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 H 2 S 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 H 2 S in improving diabetes-related diseases by regulating ER stress and carefully analyzed its mechanism in order to provide a theoretical reference for future research.

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 (H 2 S) is considered to be the third gas signal molecule after nitrous oxide and carbon monoxide. In recent years, H 2 S 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 H 2 S in regulating autophagy in liver disorders, in order to provide a basis for further research in the future.

Autophagy is a vital cell mechanism which plays an important role in many physiological processes including clearing long-lived, accumulated and misfolded proteins, removing damaged organelles and regulating growth and aging. Autophagy also participates in a variety of biological functions, such as development, cell differentiation, resistance to pathogens and nutritional hunger. Recently, autophagy has been reported to be involved in diabetes, but the mechanism is not fully understood. Hydrogen sulfide (H 2 S) is a colorless, water-soluble, flammable gas with the typical odor of rotten eggs, which has been known as a highly toxic gas for many years. However, it has been reported recently that H 2 S, together with nitric oxide and carbon monoxide, is an important gas signal transduction molecule. H 2 S has been reported to play a protective role in many diabetes-related diseases, but the mechanism is not fully clear. Recent studies indicate that H 2 S plays an important role by regulating autophagy in many diseases including cancer, tissue fibrosis diseases and glycometabolic diseases; however, the related mechanism has not been fully studied. In this review, we summarize recent research on the role of H 2 S in regulating autophagy in diabetic-related diseases to provide references for future related research.

Inflammasome is a complex composed of several proteins and an important part of the natural immune system. Nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome is composed of NLRP3, apoptosis associated speck like protein (ASC) and pro-caspase-1. It plays an important role in many diseases. Hydrogen sulfide (H 2 S) is an important signaling molecule that regulates many physiological and pathological processes. Recent studies indicated that H 2 S played anti-inflammatory and pro-inflammatory roles in many diseases through influencing NLRP3 inflammasome, but its mechanism was not fully understood. This article reviewed the progress about the effects of H 2 S on NLRP3 inflammasome and its mechanisms involved in recent years to provide theoretical basis for in-depth study., Competing Interests: Competing Interests: The authors have declared that no competing interest exists., (© The author(s).)

The endoplasmic reticulum is an important organelle responsible for protein synthesis, modification, folding, assembly and transport of new peptide chains. When the endoplasmic reticulum protein folding ability is impaired, the unfolded or misfolded proteins accumulate to lead to endoplasmic reticulum stress. Hydrogen sulfide is an important signaling molecule that regulates many physiological and pathological processes. Recent studies indicate that H 2 S plays an important protective role in many diseases through influencing endoplasmic reticulum stress, but its mechanism is not fully understood. This article reviewed the progress about the effect of H 2 S on endoplasmic reticulum stress and its mechanisms involved in diseases in recent years to provide theoretical basis for in-depth study., Competing Interests: Competing Interests: The authors have declared that no competing interest exists., (© The author(s).)

The aim of this study is to investigate whether exogenous hydrogen sulfide (H 2 S) could mitigate lipopolysaccharide (LPS) + Adenosine Triphosphate (ATP)-induced inflammation by inhibiting nucleotide-binding oligomerization domain-like receptor 3 (NLRP3) inflammasome activation and promoting autophagy in L02 cells. We stimulated L02 cells with different concentrations of LPS, then the cell viability, cell apoptosis, and the protein level of NLRP3 inflammasome were detected by MTT and western blot to determine the appropriate LPS concentration used in this study. The cells were divided into 4 group: the cells in control group were cultured with RPMI-1640 for 23.5 h; the cells in LPS + ATP group were cultured with RPMI-1640 for 0.5 h, then were stimulated with 100 ng/ml LPS for 18 h followed by stimulation with 5 mM ATP for 5 h; the cells in Sodium hydrosulfide (NaHS) + LPS + ATP group were pretreated with NaHS for 0.5 h before exposure to LPS for 18 h and ATP for 5 h; the cells in NaHS group were treated with NaHS for 0.5 h, then were cultured with RPMI-1640 for 23 h. Subsequently, the cells in each group were collected, the protein levels of NLRP3, pro-caspase-1, cleaved caspase-1, P62, toll-like receptor 4 (TLR4), nuclear factor-kappa B (NF-κB), LC3, Beclin-1, and interleukin (IL)-1 beta (β) were detected by western blot and enzyme-linked immunosorbent assay. Our results showed that exogenous H 2 S reduced the protein levels of NLRP3, cleaved caspase-1, TLR4, NF-κB, P62, and IL-1β induced by LPS + ATP and increased the ratio of LC3-II/I and the protein levels of Beclin 1 suppressed by LPS + ATP. This study demonstrated that H 2 S might suppress LPS + ATP-induced inflammation by inhibiting NLRP3 inflammasome and promoting autophagy. In conclusion, H 2 S might have potential applications in the treatment of aseptic hepatitis.

Hydrogen sulfide (H 2 S) is involved in the development and progression of many types of cancer. However, the effect and mechanism of H 2 S on the growth of human thyroid carcinoma cells remain unknown. In the present study, we found that the proliferation, viability, migration, and invasion of human thyroid carcinoma cells were enhanced by 25-50 μ M NaHS (an H 2 S donor) and inhibited by 200 μ M NaHS. However, H 2 S showed no obvious effects on the proliferation, viability, and migration of human normal thyroid cells. Administration of 50 μ M NaHS increased the expression levels of CBS, SQR, and TST, while 200 μ M NaHS showed reverse effects in human thyroid carcinoma cells. After treatment with 25-50 μ M NaHS, the ROS levels were decreased and the protein levels of p-PI3K, p-AKT, p-mTOR, H-RAS, p-RAF, p-MEK1/2, and p-ERK1/2 were increased, whereas 200 μ M NaHS exerted opposite effects in human thyroid carcinoma cells. Furthermore, 1.4-2.8 mg/kg/day NaHS promoted the tumor growth and blood vessel formation in human thyroid carcinoma xenograft tumors, while 11.2 mg/kg/day NaHS inhibited the tumor growth and angiogenesis. In conclusion, our results demonstrate that exogenous H 2 S regulates the growth of human thyroid carcinoma cells through ROS/PI3K/Akt/mTOR and RAS/RAF/MEK/ERK signaling pathways. Novel H 2 S-releasing donors/drugs can be designed and applied for the treatment of thyroid cancer.

Hydrogen sulfide (H 2 S) has been considered the third gaseous signaling molecule that plays important roles in a wide range of physiological and pathological conditions. However, there has been some controversy on the role of H 2 S in autophagy. Recent studies indicate that a number of signaling pathways are involved in the pro-autophagy effect of H 2 S, such as PI3K/Akt/mTOR, AMPK/mTOR, LKB1/STRAD/MO25, and miR-30c signaling pathways. On the other hand, there are many signaling pathways that play important roles in the anti-autophagy effect of H 2 S, including SR-A, PI3K/SGK1/GSK3β, PI3K/AKT/mTOR, Nrf2-ROS-AMPK, AMPK/mTOR, and JNK1 signaling pathways. Novel H 2 S-releasing donors/drugs could be designed and identified in order to increase the therapeutic effects by mediating autophagy in human diseases. In this review, the H 2 S metabolism in mammals is summarized and the effects of signaling pathways in H 2 S-mediated autophagy are further discussed., (Copyright © 2018. Published by Elsevier Ltd.)

Autophagy is an important cellular process, involving the transportation of cytoplasmic contents in the double membrane vesicles to lysosomes for degradation. Autophagy disorder contributes to many diseases, such as immune dysfunction, cancers and nervous system diseases. Hydrogen sulfide (H2S) is a volatile and toxic gas with a rotten egg odor. For a long time, it was considered as an environmental pollution gas. In recent years, H2S is regarded as the third most important gas signal molecule after NO and CO. H2S has a variety of biological functions and can play an important role in a variety of physiological and pathological processes. Increasingly more evidences show that H2S can regulate autophagy to play a protective role in the nervous system, but the mechanism is not fully understood. In this review, we summarize the recent literatures on the role of H2S in the pathological process of the nervous system by regulating autophagy, and analyze the mechanism in detail, hoping to provide the reference for future related research. [ABSTRACT FROM AUTHOR]