Review
Biochemistry & Molecular Biology
Bindu D. Paul, Solomon H. Snyder, Khosrow Kashfi
Summary: Hydrogen sulfide (H2S) was once thought to be only toxic, but is now known to also act as an endogenous signaling molecule. The effects of H2S on cellular physiology are dose-dependent, with lower concentrations being beneficial and higher concentrations being cytotoxic. In particular, H2S has contrasting effects on mitochondrial function, inhibiting the electron transport chain at higher concentrations and stimulating bioenergetics at lower concentrations.
Article
Plant Sciences
Xiao-Le Wang, Si-Tong Feng, Ya-Ting Wang, Ning-Ning Zhang, Zhen-Yu Guo, Xu Yan, Yu-He Yuan, Zhen-Zhen Wang, Nai-Hong Chen, Yi Zhang
Summary: This study demonstrates that mangiferin can protect against Parkinson's disease by restoring mitochondrial ultrastructure and ATP levels, reducing Drp1 expression, and modulating mitophagic proteins in a mouse model of PD.
Article
Biochemistry & Molecular Biology
Dengyu Ji, Chenghua Luo, Jing Liu, Yan Cao, Jiangxu Wu, Wenjing Yan, Ke Xue, Jiayin Chai, Xinyu Zhu, Ye Wu, Huirong Liu, Wen Wang
Summary: The study identified that hydrogen sulfide (H2S) could enhance the bioactivity of MTHFR through S-sulfhydration, offering a potential therapeutic strategy for hyperhomocysteinemia (HHcy).
ANTIOXIDANTS & REDOX SIGNALING
(2022)
Article
Cell Biology
Yifan Wang, Xiaoying Ying, Yuehong Wang, Zhiguo Zou, Ancai Yuan, Zemeng Xiao, Na Geng, ZhiQing Qiao, Wenli Li, Xiyuan Lu, Jun Pu
Summary: This study found that hydrogen sulfide (H2S) protects against doxorubicin (DOX)-induced cardiotoxicity by inhibiting ferroptosis via targeting the OPA3-NFS1 axis. This provides a potential therapeutic strategy for the treatment of DOX-induced cardiotoxicity.
CELLULAR SIGNALLING
(2023)
Article
Cell Biology
Shuo Peng, Dechao Zhao, Qianzhu Li, Mengyi Wang, Shiwu Zhang, Kemiao Pang, Jiayi Huang, Fanghao Lu, He Chen, Weihua Zhang
Summary: This study found that exogenous H2S affects cellular calcium transport by regulating the H2S/MuRF1/SERCA2a/cardiac contractile pathway. Exogenous H2S restored the protein expression levels and activity of CSE and SERCA2a, while reducing cytosolic calcium concentrations and MuRF1 expression. NaHS administration modified MuRF1 S-sulfhydration and enhanced the activity and expression of SERCA2a.
Article
Medicine, Research & Experimental
Shuo Peng, Mengyi Wang, Shiwu Zhang, Ning Liu, Qianzhu Li, Jiaxin Kang, Lingxue Chen, Mingyu Li, Kemiao Pang, Jiayi Huang, Fanghao Lu, Dechao Zhao, Weihua Zhang
Summary: The aim of this study was to determine whether H2S regulates intracellular calcium homeostasis by acting on SERCA2a to reduce cardiomyocyte apoptosis during DCM. The results showed that exogenous H2S elevates SENP1 S-sulfhydration to increase SERCA2a SUMOylation, improve myocardial systolic-diastolic function, and decrease cardiomyocyte apoptosis in DCM.
BIOMEDICINE & PHARMACOTHERAPY
(2023)
Article
Cardiac & Cardiovascular Systems
Zhao-Yang Lu, Chun-Ling Guo, Bin Yang, Yao Yao, Zhuo-Jing Yang, Yu-Xin Gong, Jing-Yao Yang, Wen-Yuan Dong, Jun Yang, Hai-Bing Yang, Hui-Min Liu, Bao Li
Summary: This study demonstrated that exogenous H2S treatment can suppress TGF-beta 1-induced activation of adventitial fibroblasts by regulating mitochondrial fission and reactive oxygen species generation.
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY
(2022)
Article
Biology
Rebecca A. Ellwood, Luke Slade, Jonathan Lewis, Roberta Torregrossa, Surabhi Sudevan, Mathew Piasecki, Matthew Whiteman, Timothy Etheridge, Nathaniel J. Szewczyk
Summary: A C. elegans model of Duchenne muscular dystrophy suggests that disrupted sulfur metabolism may play a role in the disease. By supplementing sulfur containing amino acids, the deficit in hydrogen sulfide levels can be mitigated, leading to improved muscle health through various mechanisms. The study also highlights differences in protection mechanisms between sulfur amino acid and H2S administration.
COMMUNICATIONS BIOLOGY
(2022)
Article
Multidisciplinary Sciences
Daniel Giovinazzo, Biljana Bursac, Juan Sbodio, Sumedha Nalluru, Thibaut Vignane, Adele M. Snowman, Lauren M. Albacarys, Thomas W. Sedlak, Roberta Torregrossa, Matthew Whiteman, Milos R. Filipovic, Solomon H. Snyder, Bindu D. Paul
Summary: Alzheimer's disease is characterized by memory, executive, and motor function deterioration, with neuropathological hallmarks including neurofibrillary tangles, paired helical filaments, and amyloid plaques. Dysregulation of signaling by hydrogen sulfide has been shown during aging and may play a role in preventing hyperphosphorylation of Tau in Alzheimer's disease. Furthermore, administering the H2S donor sodium GYY4137 to mouse models of Alzheimer's disease has been shown to ameliorate motor and cognitive deficits associated with the disease.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
(2021)
Article
Microbiology
Hongou Wang, Qianrui Bai, Guodong Ma
Summary: As an important endogenous signaling molecule, hydrogen sulfide can induce reversible post-translational modifications on cysteine residues of proteins, forming a persulfide bond called S-sulfhydration. Understanding the biofunctions of S-sulfhydration will help us characterize its regulatory roles in various physiological processes and diseases. However, the current understanding of S-sulfhydration mainly relies on mammalian cells and animal models, and its effects on bacteria are summarized in this study. The development of sensitive and high-throughput detection technologies is crucial for studying the signal transduction mechanism of H2S and protein S-sulfhydration modification.
MICROBIOLOGICAL RESEARCH
(2023)
Article
Cardiac & Cardiovascular Systems
Zhen Li, Huijing Xia, Thomas E. Sharp, Kyle B. LaPenna, John W. Elrod, Kevin M. Casin, Ken Liu, John W. Calvert, Vinh Q. Chau, Fadi N. Salloum, Shi Xu, Ming Xian, Noriyuki Nagahara, Traci T. Goodchild, David J. Lefer
Summary: This study reveals that the reduction of 3-MST in the myocardium is associated with heart failure. Knockout of 3-MST worsens cardiac and vascular dysfunction in a mouse model of pressure overload-induced heart failure. Restoring branched-chain amino acid metabolism and administrating an H2S donor can alleviate the detrimental effects of 3-MST deficiency in heart failure.
CIRCULATION RESEARCH
(2022)
Article
Biochemistry & Molecular Biology
Chenghua Luo, Dengyu Ji, Yan Li, Yan Cao, Shangyue Zhang, Wenjing Yan, Ke Xue, Jiayin Chai, Ye Wu, Huirong Liu, Wen Wang
Summary: This study revealed a new mechanism of post-translational modification of Sp1/CSE, investigated the specific effects of homocysteine metabolism disorder on H2S deficiency, and proposed therapeutic strategies involving restoring S-sulfhydration and blocking nitration.
FREE RADICAL BIOLOGY AND MEDICINE
(2021)
Article
Nutrition & Dietetics
Kelin Li, Minghui Wang, Ruxia Wang, Xiaojuan Wang, Hongchao Jiao, Jingpeng Zhao, Yunlei Zhou, Haifang Li, Hai Lin
Summary: This study reveals the role of hydrogen sulfide (H2S) in enhancing glucose uptake and utilization in chicks. The results suggest that NaHS is involved in glucose uptake in skeletal muscle in a fiber type-dependent way. The AMPK/p38 pathway and protein S-sulfhydration promote glucose uptake in fast-twitch glycolytic muscle fibers, which provides a muscle fiber-specific potential therapeutic target to ameliorate glucose metabolism.
JOURNAL OF NUTRITION
(2023)
Article
Multidisciplinary Sciences
Luis Rios, Suman Pokhrel, Sin-Jin Li, Gwangbeom Heo, Bereketeab Haileselassie, Daria Mochly-Rosen
Summary: The researchers have identified a small molecule that can mimic the effects of a peptide inhibitor and reduce the burden of protein-related diseases. This study is important for understanding and potentially treating various pathologies associated with protein dysregulation.
NATURE COMMUNICATIONS
(2023)
Article
Cell Biology
Xiangyu Mao, Yihua Gu, Xiangyu Sui, Lei Shen, Jun Han, Haiyu Wang, Qiulei Xi, Qiulin Zhuang, Qingyang Meng, Guohao Wu
Summary: Patients with cachexia exhibit noticeable mitochondrial abnormalities and muscle loss, with an imbalance in mitochondrial dynamics potentially contributing to muscle atrophy. Regulation of DRP1 could ameliorate these abnormalities caused by cachexia.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)