Physiological implications of hydrogen sulfide: a whiff exploration that blossomed.
- Rui Wang
- BiologyPhysiological Reviews
- 1 April 2012
The important life-supporting role of hydrogen sulfide (H(2)S) has evolved from bacteria to plants, invertebrates, vertebrates, and finally to mammals. Over the centuries, however, H(2)S had only…
H2S as a Physiologic Vasorelaxant: Hypertension in Mice with Deletion of Cystathionine γ-Lyase
It is shown that H2S is physiologically generated by cystathionine γ-lyase (CSE) and that genetic deletion of this enzyme in mice markedly reduces H 2S levels in the serum, heart, aorta, and other tissues.
H2S Signals Through Protein S-Sulfhydration
Ex vivo endogenous H2S physiologically modifies cysteine residues in many proteins, including glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and actin, converting Cysteine -SH groups to -SSH groups in a process the authors call S-sulfhydration.
Carbon Monoxide: Endogenous Production, Physiological Functions, and Pharmacological Applications
Understanding of the cellular and molecular mechanisms that regulate the production and mediate the physiological actions of CO has greatly advanced and many diseases, including neurodegenerations, hypertension, heart failure, and inflammation, have been linked to the abnormality in CO metabolism and function.
Hydrogen Sulfide as Endothelium-Derived Hyperpolarizing Factor Sulfhydrates Potassium Channels
H2S is a major EDHF that causes vascular endothelial and smooth muscle cell hyperpolarization and vasorelaxation by activating the ATP-sensitive, intermediate conductance and small conductance potassium channels through cysteine S-sulfhydration.
Hydrogen sulfide is an endogenous stimulator of angiogenesis
- A. Papapetropoulos, A. Pyriochou, C. Szabó
- BiologyProceedings of the National Academy of Sciences
- 22 December 2009
Investigation of the role of exogenous and endogenous hydrogen sulfide on neovascularization and wound healing in vitro and in vivo concludes that endogenous and exogenous H2S stimulates EC-related angiogenic properties through a KATP channel/MAPK pathway.
Hydrogen sulfide protects against cellular senescence via S-sulfhydration of Keap1 and activation of Nrf2.
These results provide a mechanistic insight into how H2S signaling mediates cellular senescence induced by oxidative stress and protects against cellular aging via S-sulfhydration of Keap1 and Nrf2 activation in association with oxidative stress.
H2S Protects Against Pressure Overload–Induced Heart Failure via Upregulation of Endothelial Nitric Oxide Synthase
H2S levels are decreased in mice in the setting of heart failure, and oral H2S therapy prevents the transition from compensated to decompensated heart failure in part via upregulation of endothelial nitric oxide synthase and increased Nitric oxide bioavailability.
Decreased Endogenous Production of Hydrogen Sulfide Accelerates Atherosclerosis
Endogenously synthesized H2S protects vascular tissues from atherogenic damage by reducing vessel intimal proliferation and inhibiting adhesion molecule expression.
Hydrogen sulfide-based therapeutics: exploiting a unique but ubiquitous gasotransmitter
Animal studies of several H2S-releasing drugs have demonstrated considerable promise for the safe treatment of a wide range of disorders, and several such drugs are now in clinical trials.