20 results on '"Guangdong Yang"'
Search Results
2. Research on Risk Assessment and Control for Urban Rainwater Resources Utilization.
- Author
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Zhang, L., Defilla, S., Chu, W., Li, Qin, Chengxiang, Ma, Junde, Wang, Yanzhao, Jin, and Guangdong, Yang
- Published
- 2021
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3. Interaction among estrogen, IGF-1, and H2S on smooth muscle cell proliferation.
- Author
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Tian Shuang, Ming Fu, Guangdong Yang, Ying Huang, Zhongming Qian, Lingyun Wu, and Rui Wang
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SMOOTH muscle ,MUSCLE cells ,VASCULAR smooth muscle ,CELL proliferation ,ESTROGEN ,ESTROGEN antagonists ,ESTROGEN receptors - Abstract
Both estrogen and hydrogen sulfide (H
2 S) inhibit the proliferation of vascular smooth muscle cells (SMCs) and development of atherosclerosis. In the absence of endogenous H2 S as occurred in CSE-knockout (KO) mouse, however, estrogen stimulates the proliferation of vascular SMCs. The underlying mechanisms for this seemingly controversial vascular effect of estrogen are unclear. In the present study, we demonstrated that the stimulatory effect of estrogen on the p roliferation of CSE-KO SMCs was suppressed by the inhibitor of insulin-like growth fac tor-1 receptor (IGF-1R) or knockdown of IGF-1R protein expression. Estrogen downregulat ed the expression of insulin-like growth factor-1 (IGF-1) and IGF-1R in aortic tissu es or aortic SMCs isolated from WT and CSE-KO mice. Furthermore, endogenous H2 S downregulated IGF-1R, but upregulated estrogen receptor (ER)-α, in aortic tissues or SMCs. ER-α and IGF-1R were co-located in SMCs and co-immunoprecipitated, which was decreas ed by H2 S. Finally, both endogenous and exogenous H2 S induced the S-sulfhydration of IGF-1R, but not ER-α, in WT-SMCs and CSE-KO SMCs, which underlies the decreased for mation of IGF-1R/ER-α hybrid in the presence of H2 S. Thus, the absence of H2 S favors the interaction of estrogen with IGF-1R/ER-α hybrid to stimulate SMCs proliferation. The appreciation of a critical role of H2 S in preventing estrogen-induced SMCs proliferation will help b etter understand the regulation of complex vascular effects of estroge n and sex-related cardiovascular diseases. [ABSTRACT FROM AUTHOR]- Published
- 2021
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4. H2S as a potential defense against COVID-19?
- Author
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Guangdong Yang
- Subjects
COVID-19 ,SARS-CoV-2 ,COVID-19 pandemic ,ANGIOTENSIN converting enzyme - Abstract
The outbreak of COVID-19 pneumonia caused by a new coronavirus (severe acute respiratory syndrome coronavirus 2, SARS-CoV-2) is posing a global health emergency and has led to more than 380,000 deaths worldwide. The cell entry of SARS-CoV-2 depends on two host proteins angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2). There is currently no vaccine available and also no effective drug for the treatment of COVID-19. Hydrogen sulfide (H
2 S) as a novel gasotransmitter has been shown to protect against lung damage via its anti-inflammation, antioxidative stress, antiviral, prosurvival, and antiaging effects. In light of the research advances on H2 S signaling in biology and medicine, this review proposed H2 S as a potential defense against COVID-19. It is suggested that H2 S may block SARS-CoV-2 entry into host cells by interfering with ACE2 and TMPRSS2, inhibit SARS-CoV-2 replication by attenuating virus assembly/release, and protect SARS-CoV-2-induced lung damage by suppressing immune response and inflammation development. Preclinical studies and clinical trials with slow-releasing H2 S donor(s) or the activators of endogenous H2 S-generating enzymes should be considered as a preventative treatment or therapy for COVID-19. [ABSTRACT FROM AUTHOR]- Published
- 2020
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5. Trend in H2S Biology and Medicine Research--A Bibliometric Analysis.
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Guangdong Yang and Lingyun Wu
- Subjects
HYDROGEN sulfide ,BIOLOGICAL research ,BIBLIOMETRICS ,DATABASES ,CARDIOVASCULAR system - Abstract
The biological and medical importance of hydrogen sulfide (H
2 S) has been recognized for decades. The aim of this bibliometric study is to analyze the quantity and quality of publications in H2 S biology and medicine (H2 SBM) based on the databases of Web of Science and Google Scholar. A total of 5881 publications published between 1990 and2 016 were analyzed. The number of H2 SBM papers published before 2004 was below 100 annually, but thereafter this number rapidly increased and peaked in 2015 with more than 7-fold increase. All publications related to H2 SBM research achieved a total h-index of 136 and were cited 123,074 times. The most published disciplines in H2 S biomedicine research were the cardiovascular system (8.5%), neuroscience (6.5%), and gastroenterology hepatology (4.7%). The country with the greatest number of publications in the H2 SBM research field was the USA with 1765 (30.0%) publications, followed by China with 995 (16.9%) publications and Japan with 555 (9.4%) publications. The top 3 most published institutes were National University of Singapore, Peking University in China, and University of Groningen in Netherlands. Nitric Oxide Biology and Chemistry was the most exploited journal for H2 SBM publications with 461 articles, followed by FASEB Journal with 200 publications and Antioxidants Redox Signaling with 116 publications. The most highly cited publications and researchers in H2 SBM research were also unmasked from this bibliometric analysis. Collectively, H2 SBM publications exhibit a continuous trend of increase, reflecting the increased H2 SBM research intensity and diversity globally. [ABSTRACT FROM AUTHOR]- Published
- 2017
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6. H2S-Mediated Protein S-Sulfhydration: A Prediction for Its Formation and Regulation.
- Author
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Youngjun Ju, Ming Fu, Stokes, Eric, Lingyun Wu, and Guangdong Yang
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PROTEIN S ,CYSTEINE proteinases ,NITRIC oxide ,VITAMIN K-dependent proteins ,NITROSYLATION - Abstract
Protein S-sulfhydration is a newly discovered post-translational modification of specific cysteine residue(s) in target proteins, which is involved in a broad range of cellular functions and metabolic pathways. By changing local conformation and the final activity of target proteins, S-sulfhydration is believed to mediate most cellular responses initiated by H
2 S, a novel gasotransmitter. In comparison to protein S-sulfhydration, nitric oxide-mediated protein S-nitrosylation has been extensively investigated, including its formation, regulation, transfer and metabolism. Although the investigation on the regulatory mechanisms associated with protein S-sulfhydration is still in its infancy, accumulated evidence suggested that protein S-sulfhydration may share similar chemical features with protein S-nitrosylation. Glutathione persulfide acts as a major donor for protein S-sulfhydration. Here, we review the present knowledge on protein S-sulfhydration, and also predict its formation and regulation mechanisms based on the knowledge from protein S-nitrosylation. [ABSTRACT FROM AUTHOR]- Published
- 2017
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7. Exogenous H2S contributes to recovery of ischemic post-conditioning-induced cardioprotection by decrease of ROS level via down-regulation of NF-κB and JAK2-STAT3 pathways in the aging cardiomyocytes.
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Lina Li, Meixiu Li, Youyou Li, Weiming Sun, Yuehong Wang, Shuzhi Bai, Hongxia Li, Bo Wu, Guangdong Yang, Rui Wang, Lingyun Wu, Hongzhu Li, and Changing Xu
- Subjects
HYDROGEN sulfide ,HYPOXIA-inducible factors ,HEART cells - Abstract
Background: Hydrogen sulfide (H
2 S), a third member of gasotransmitter family along with nitric oxide and carbon monoxide, generated from mainly catalyzed by cystathionine-lyase, possesses important functions in the cardiovascular system. Ischemic post-conditioning (PC) strongly protects against the hypoxia/reoxygenation (H/R)-induced injury and apoptosis of cardiomyocytes. However, PC protection is ineffective in the aging cardiomyocytes. Whether H2 S restores PC-induced cardioprotection by decrease of reactive oxygen species (ROS) level in the aging cardiomyocytes is unknown. Methods: The aging cardiomyocytes were induced by treatment of primary cultures of neonatal cardiomyocytes using d-galactose and were exposed to H/R and PC protocols. Cell viability was observed by CCK-8 kit. Apoptosis was detected by Hoechst 33342 staining and flow cytometry. ROS level was analyzed using spectrofluorimeter. Related protein expressions were detected through Western blot. Results: Treatment of NaHS (a H2 S donor) protected against H/R-induced apoptosis, cell damage, the expression of cleaved caspase-3 and cleaved caspase-9, the release of cytochrome c (Cyt c). The supplementation of NaHS also decreased the activity of LDH and CK, MDA contents, ROS levels and the phosphorylation of IκBα, NF-κB, JNK2 and STAT3, and increased cell viability, the expression of Bcl-2, the activity of SOD, CAT and GSH-PX. PC alone did not provide cardioprotection in H/R-treated aging cardiomyocytes, which was significantly restored by the addition of NaHS. The beneficial role of NaHS was similar to the supply of N-acetyl-cysteine (NAC, an inhibitor of ROS), Ammonium pyrrolidinedithiocarbamate (PDTC, an inhibitor of NF-κB) and AG 490 (an inhibitor of JNK2), respectively, during PC. Conclusion: Our results suggest that exogenous H2 S contributes to recovery of PC-induced cardioprotection by decrease of ROS level via down-regulation of NF-κB and JAK2/STAT3 pathways in the aging cardiomyocytes. [ABSTRACT FROM AUTHOR]- Published
- 2016
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8. The coordination of S-sulfhydration, S-nitrosylation, and phosphorylation of endothelial nitric oxide synthase by hydrogen sulfide.
- Author
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Altaany, Zaid, YoungJun Ju, Guangdong Yang, and Rui Wang
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- 2014
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9. Oxygen-sensitive mitochondrial accumulation of cystathionine β-synthase mediated by Lon protease.
- Author
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Huajian Teng, Bo Wu, Kexin Zhao, Guangdong Yang, Lingyun Wu, and Rui Wang
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CYSTATHIONINE ,PROTEASE inhibitors ,OXYGEN detectors ,HEMOPROTEINS ,HYDROGEN sulfide - Abstract
Oxygen-sensitive accumulation and degradation, two opposite but intrinsically linked events, of heme proteins in mitochondria affect mitochondrial functions, including bioenergetics and oxygen-sensing processes. Cystathionine β-synthase (CBS) contains a prosthetic heme group and catalyzes the production of hydrogen sulfide in mammalian cells. Here we show that CBS proteins were present in liver mitochondria at a low level under normoxia conditions. Ischemia/hypoxia increased the accumulation of CBS proteins in mitochondria. The normalization of oxygen partial pressure accelerated the degradation of CBS proteins. Lon protease, a major degradation enzyme in mitochondrial matrix, recognized and degraded mitochondrial CBS by specifically targeting at the oxygenated heme group of CBS proteins. The accumulation of CBS in mitochondria increased hydrogen sulfide production, which prevented Ca
2+ -mediated cytochrome c release from mitochondria and decreased reactive oxygen species generation. Mitochondrial accumulation of heme oxygenase-1, another heme protein, was also regulated by oxygen level and Lon protease in the same mechanism as for CBS. Our findings provide a fundamental and general mechanism for oxygen-sensitive regulation of mitochondrial functions by linking oxygenation level to the accumulation/ degradation of mitochondrial heme proteins. [ABSTRACT FROM AUTHOR]- Published
- 2013
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10. Decreased Endogenous Production of Hydrogen Sulfide Accelerates Atherosclerosis.
- Author
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Mani, Sarathi, Hongzhu Li, Untereiner, Ashley, Lingyun Wu, Guangdong Yang, Austin, Richard C., Dickhout, Jeffrey G., Lhoták, Šárka, Meng, Qing H., and Rui Wang
- Published
- 2013
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11. H2S signaling in redox regulation of cellular functions.
- Author
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Youngjun Ju, Weihua Zhang, Yanxi Pei, and Guangdong Yang
- Subjects
HYDROGEN sulfide ,OXIDATION-reduction reaction ,CYTOLOGICAL research ,OXIDATIVE stress ,GLUTATHIONE ,OLIGOPEPTIDES ,CYSTATHIONINE gamma-lyase ,LYASES - Abstract
Copyright of Canadian Journal of Physiology & Pharmacology is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
- Published
- 2013
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12. Interaction of Hydrogen Sulfide and Estrogen on the Proliferation of Vascular Smooth Muscle Cells.
- Author
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Hongzhu Li, Sarathi Mani, Wei Cao, Guangdong Yang, Christopher Lai, Lingyun Wu, Rui Wang, and Tianqing Peng
- Subjects
CYSTATHIONINE gamma-lyase ,HYDROGEN sulfide ,CARDIOVASCULAR system ,ESTROGEN ,CELL proliferation ,LABORATORY mice - Abstract
Hydrogen sulfide (H
2 S) can be endogenously generated from cystathionine gamma-lyase (CSE) in cardiovascular system, offering a cardiovascular protection. It is also known that the lower risk of cardiovascular diseases in female is partially attributed to the protective effect of estrogen. The current study explores the interaction of H2 S and estrogen on smooth muscle cell (SMC) growth. In the present study, we found that the proliferation of cultured vascular SMCs isolated from wild-type mice (WT-SMCs) was inhibited, but that from CSE gene knockout mice (CSE-KO-SMCs) increased, by estrogen treatments. The expression of estrogen receptor α (ERα), but not ERβ, was significantly decreased in CSE-KO-SMCs compared with that in WT-SMCs. Exogenously applied H2 S markedly increased ERα but not ERβ expression. In addition, the inhibition of ER activation and knockdown of ERα expression in WT-SMCs or the overexpression of ERα in CSE-KO-SMCs reversed the respective effects of estrogen on cell proliferation. The expression of cyclin D1 was reduced in WT- SMCs but increased in CSE-KO-SMCs after estrogen treatments, which was reversed by knockdown of ERα in WT-SMCs or overexpression of ERα in CSE-KO- SMCs, respectively. The overexpression of cyclin D1 in WT-SMCs or knockdown of cyclin D1 expression in CSE-KO-SMCs reversed the effects of estrogen on cell proliferation. These results suggest that H2 S mediates estrogen- inhibited proliferation of SMCs via selective activation of ERα/cyclin D1 pathways. [ABSTRACT FROM AUTHOR]- Published
- 2012
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13. Hydrogen sulfide (H2S) metabolism in mitochondria and its regulatory role in energy production.
- Author
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Ming Fu, Weihua Zhang, Lingyun Wu, Guangdong Yang, Hongzhu Li, and Rui Wang
- Subjects
HYDROGEN sulfide ,MITOCHONDRIA ,CONFOCAL microscopy ,CYSTATHIONINE ,GREEN fluorescent protein ,ADENOSINE triphosphate ,MUSCLE cells - Abstract
Although many types of ancient bacteria and archea rely on hydrogen sulfide (H
2 S) for their energy production, eukaryotes generate ATP in an oxygen-dependent fashion. We hypothesize that endogenous H2 S remains a regulator of energy production in mammalian cells under stress conditions, which enables the body to cope with energy demand when oxygen supply is insufficient. Cystathionine γ-lyase (CSE) is a major H2 S-producing enzyme in the cardiovascular system that uses cysteine as the main substrate. Here we show that CSE is localized only in the cytosol, not in mitochondria, of vascular smooth-muscle cells (SMCs) under resting conditions, revealed by Western blot analysis and confocal microscopy of SMCs transfected with GFP-tagged CSE plasmid. After SMCs were exposed to A23187, thapsigargin, or tunicamycin, intracellular calcium level was increased, and CSE translocated from the cytosol to mitochondria. CSE was coimmunoprecipitated with translocase of the outer membrane 20 (Tom20) in mitochondrial membrane. Tom20 siRNA significantly inhibited mitochondrial translocation of CSE and mitochondrial H2 S production. The cysteine level inside mitochondria is approximately three times that in the cytosol. Translocation of CSE to mitochondria metabolized cysteine, produced H2 S inside mitochondria, and increased ATP production. Inhibition of CSE activity reversed A23187-stimulated mitochondrial ATP production. H2 S improved mitochondrial ATP production in SMCs with hypoxia, which alone decreased ATP production. These results suggest that translocation of CSE to mitochondria on specific stress stimulations is a unique mechanism to promote H2 S production inside mitochondria, which subsequently sustains mitochondrial ATP production under hypoxic conditions. [ABSTRACT FROM AUTHOR]- Published
- 2012
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14. Hydrogen sulfide in cell survival: a double-edged sword.
- Author
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Guangdong Yang
- Subjects
HYDROGEN sulfide ,REGULATION of cell growth ,ANTINEOPLASTIC agents ,PHARMACEUTICAL research ,NEUROTRANSMITTERS - Abstract
Hydrogen sulfide (H
2 S) has been found to play an important role as a signal molecule in regulating cell survival. It appears paradoxical that, on one side, H2 S acts as a physiological intercellular messenger to stimulate cell growth, and on the other side, it may display cytotoxic activity. This article summarizes the current body of evidence demonstrating the cytoprotective versus cytotoxic effects of H2 S in mammalian cells and describes the janus-faced properties of this important gasotransmitter. This article will also provide a brief description of the current signaling mechanisms that have been demonstrated to be responsible for these different actions. The pharmacologic regulation of H2 S production and the potential clinical significance of H2 S are highlighted. [ABSTRACT FROM AUTHOR]- Published
- 2011
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15. Cystathionine gamma-lyase deficiency and overproliferation of smooth muscle cells.
- Author
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Guangdong Yang, Lingyun Wu, Bryan, Sean, Khaper, Neelam, Mani, Sarathi, and Rui Wang
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SMOOTH muscle ,MUSCLE cells ,CYSTATHIONINE gamma-lyase ,HYDROGEN sulfide ,APOPTOSIS ,HYPERTENSION - Abstract
Aims: Cystathionine gamma-lyase (CSE)-derived H2S plays an important role in regulating cell growth. Lack of CSE expression results in development of hypertension. The current study compared proliferation of smooth muscle cells derived from CSE gene knockout mice (SMCs-KO) with that of wild-type mice (SMCs-WT). [ABSTRACT FROM PUBLISHER]
- Published
- 2010
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16. Hydrogen sulfide as an oxygen sensor in trout gill chemoreceptors.
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Olson, Kenneth R., Healy, Michael J., Zhaohong Qin, Skovgaard, Nini, Vulesevic, Branka, Duff, Douglas W., Whitfield, Nathan L., Guangdong Yang, Rui Wang, and Perry, Steve F.
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HYDROGEN sulfide ,CHEMORECEPTORS ,SENSORY receptors ,VASCULAR smooth muscle ,GILLS - Abstract
O
2 chemoreceptors elicit cardiorespiratory reflexes in all vertebrates, but consensus on O2 -sensing signal transduction mechanism(s) is lacking. We recently proposed that hydrogen sulfide (H2 S) metabolism is involved in O2 sensing in vascular smooth muscle. Here, we examined the possibility that H2 S is an O2 sensor in trout chemoreceptors where the first pair of gills is a primary site of aquatic O2 sensing and the homolog of the mammalian carotid body. Intrabuccal injection of H2 S in unanesthetized trout produced a dose-dependent bradycardia and increased ventilatory frequency and amplitude similar to the hypoxic response. Removal of the first, but not second, pair of gills significantly inhibited H2 S-mediated bradycardia, consistent with the loss of aquatic chemoreceptors. mRNA for H2 S-synthesizing enzymes, cystathionine &x#03B2;-synthase and cystathionine-&x#03B3;-lyase, was present in branchial tissue. Homogenized gills produced H2 S enzymatically, and H2 S production was inhibited by O2 , whereas mitochondrial H2 S consumption was O2 dependent. Ambient hypoxia did not affect plasma H2 S in unanesthetized trout, but produced a Po2 -dependent increase in a sulfide moiety suggestive of increased H2 S production. In isolated zebrafish neuroepithelial cells, the putative chemoreceptive cells of fish, both hypoxia and H2 S, produced a similar ~10-mV depolarization. These studies are consistent with H2 S involvement in O2 sensing/signal transduction pathway(s) in chemoreceptive cells, as previously demonstrated in vascular smooth muscle. This novel mechanism, whereby H2 S concentration ([H2 S]) is governed by the balance between constitutive production and oxidation, tightly couples tissue [H2 S] to Po2 and may provide an exquisitely sensitive, yet simple, O2 sensor in a variety of tissues. [ABSTRACT FROM AUTHOR]- Published
- 2008
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17. Activation of KATP channels by H2S in rat insulin-secreting cells and the underlying mechanisms.
- Author
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Wei Yang, Guangdong Yang, Xuming Jia, Lingyun Wu, and Rui Wang
- Subjects
INSULIN ,CELL lines ,CELLS ,PANCREATIC secretions ,RATS - Abstract
H
2 S is an important gasotransmitter, generated in mammalian cells from l-cysteine metabolism. As it stimulates KATP channels in vascular smooth muscle cells, H2 S may also function as an endogenous opener of KATP channels in INS-1E cells, an insulin-secreting cell line. In the present study, KATP channel currents in INS-1E cells were recorded using the whole-cell and single-channel recording configurations of the patch-clamp technique. KATP channels in INS-1E cells have a single-channel conductance of 78 pS. These channels were activated by diazoxide and inhibited by gliclazide. ATP (3 m m) in the pipette solution inhibited KATP channels in INS-1E cells. Significant amount of H2 S was produced from INS-1E cells in which the expression of cystathinonie gamma-lyase (CSE) was confirmed. After INS-1E cells were transfected with CSE-targeted short interfering RNA (CSE-siRNA) or treated with dl-propargylglycine (PPG; 1–5 m m) to inhibit CSE, endogenous production of H2 S was abolished. Increase in extracellular glucose concentration significantly decreased endogenous production of H2 S in INS-1E cells, and increased insulin secretion. After transfection of INS-1E cells with adenovirus containing the CSE gene (Ad-CSE) to overexpress CSE, high glucose-stimulated insulin secretion was virtually abolished. Basal KATP channel currents were significantly reduced after incubating INS-1E cells with a high glucose concentration (16 m m) or lowering endogenous H2 S level by CSE-siRNA transfection. Under these conditions, exogenously applied H2 S significantly increased whole-cell KATP channel currents at concentrations equal to or lower than 100 μ m. H2 S (100 μ m) markedly increased open probability by more than 2-fold of single KATP channels (inside-out recording) in native INS-1E cells ( n= 4, P < 0.05). Single-channel conductance and ATP sensitivity of KATP channels were not changed by H2 S. In conclusion, endogenous H2 S production from INS-1E cells varies with in vivo conditions, which significantly affects insulin secretion from INS-1E cells. H2 S stimulates KATP channels in INS-1E cells, independent of activation of cytosolic second messengers, which may underlie H2 S-inhibited insulin secretion from these cells. Interaction among H2 S, glucose and the KATP channel may constitute an important and novel mechanism for the fine control of insulin secretion from pancreatic β-cells. [ABSTRACT FROM AUTHOR]- Published
- 2005
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18. Cystathionine gamma-lyase/H2S signaling facilitates myogenesis under aging and injury condition.
- Author
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Yanjie Zhang, Masters, Laura, Yuehong Wang, Lingyun Wu, Yanxi Pei, Baoqing Guo, Parissenti, Amadeo, Lees, Simon J., Rui Wang, and Guangdong Yang
- Published
- 2021
- Full Text
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19. Pro-apoptotic effect of endogenous H2S on human aorta smooth muscle cells.
- Author
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Guangdong Yang, Lingyun Wu, and Rui Wang
- Subjects
CELL proliferation ,MITOGEN-activated protein kinases ,APOPTOSIS ,MUSCLE cells ,SMOOTH muscle - Abstract
Presents findings of a study which tested the hypothesis that endogenously produced H
2 S plays a fundamental role in cell proliferation and survival. Effect of overexpressed cystathione gamma-lyase (CSE) on H2 S production and human aorta smooth muscle cell (HASMC); Role of CSE overexpression in activating mitogen-activated protein kinases and cell cycle proteins; Approach used in exploring the effect of CSE on HASMC apoptosis.- Published
- 2006
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20. Hydrogen sulfide-induced apoptosis of human aorta smooth muscle cells via the activation of mitogen-activated protein kinases and caspase-3.
- Author
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Guangdong Yang, Xianfeng Sun, and Rui Wang
- Subjects
HYDROGEN sulfide ,APOPTOSIS ,CELLULAR signal transduction ,SMOOTH muscle ,MUSCLE cells ,PHOSPHORYLATION ,PROTEIN kinases - Abstract
Discusses a study which examined the physiological role of hydrogen sulfide in the regulation of cellular apoptosis and underlying cellular signal transduction pathways. Effect of endogenous and exogenous hydrogen sulfide on human aortic smooth muscle cell apoptosis; Influence of hydrogen sulfide on the phosphorylation and activation of mitogen-activated protein kinases; Schematic signal transduction pathways underlying the hydrogen sulfide-induced apoptosis.
- Published
- 2004
- Full Text
- View/download PDF
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