ArticlePloS one2013
H(2)S inhibits hyperglycemia-induced intrarenal renin-angiotensin system activation via attenuation of reactive oxygen species generation.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 85 citations in OpenAlex.
- The Role of Ferroptosis in Diabetes Pathogenesis: Therapeutic Implications of Hydrogen Sulfide and Its Reactive Metabolites.Antioxidants (Basel, Switzerland) · 2026Review
- Co-administration of subtherapeutic doses of yohimbine and NaHS potentially ameliorates CKD-induced necroptosis by modulating RAAS/ROS imbalance, sympathetic overactivity, and inflammation.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Steam-Driven Structural Remodeling ofFoods (Basel, Switzerland) · 2026Article
- Diabetic nephropathy: Role of nitric oxide.Nitric oxide : biology and chemistry · 2025Review
- Article
- Neuroprotective Effects of a Hydrogen Sulfide Donor in Streptozotocin-Induced Diabetic Rats.International journal of molecular sciences · 2023Article
- The effect of zofenopril on the cardiovascular system of spontaneously hypertensive rats treated with the ACE2 inhibitor MLN-4760.Biological research · 2023Article
- Sulfur-Containing Amino Acids, Hydrogen Sulfide, and Sulfur Compounds on Kidney Health and Disease.Metabolites · 2023Review
- An emerging view on vascular fibrosis molecular mediators and relevant disorders: from bench to bed.Frontiers in cardiovascular medicine · 2023Review
- Hydrogen sulfide alleviates hypothyroidism-induced myocardial fibrosis in rats through stimulating autophagy and inhibiting TGF-β1/Smad2 pathway.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023Article
- The roles of hydrogen sulfide in renal physiology and disease states.Renal failure · 2022Review
- Elemental Sulfur Inhibits Yeast Growth via Producing Toxic Sulfide and Causing Disulfide Stress.Antioxidants (Basel, Switzerland) · 2022Article
- The Pathophysiology of HBiomolecules · 2022Review
- Effects of Sodium Thiosulfate During Resuscitation From Trauma-and-Hemorrhage in Cystathionine-γ-Lyase Knockout Mice With Diabetes Type 1.Frontiers in medicine · 2022Article
- Hydrogen Sulfide and the Kidney.Advances in experimental medicine and biology · 2021Article
- Hydrogen Sulfide and Carnosine: Modulation of Oxidative Stress and Inflammation in Kidney and Brain Axis.Antioxidants (Basel, Switzerland) · 2020Review
- HAmerican journal of physiology. Cell physiology · 2020Review
- Hydrogen Sulfide: Recent Progression and Perspectives for the Treatment of Diabetic Nephropathy.Molecules (Basel, Switzerland) · 2019Review
- Hydrogen sulfide-mediated regulation of cell death signaling ameliorates adverse cardiac remodeling and diabetic cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2019Review
- Melatonin ameliorates intrarenal renin-angiotensin system in a 5/6 nephrectomy rat model.Clinical and experimental nephrology · 2018Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Decrease in endogenous hydrogen sulfide (H2S) was reported to participate in the pathogenesis of diabetic nephropathy (DN). This study is aimed at exploring the relationship between the abnormalities in H2S metabolism, hyperglycemia-induced oxidative stress and the activation of intrarenal renin-angiotensin system (RAS). Cultured renal mesangial cells (MCs) and streptozotocin (STZ) induced diabetic rats were used for the studies. The expressions of angiotensinogen (AGT), angiotensin converting enzyme (ACE), angiotensin II (Ang II) type I receptor (AT1), transforming growth factor-β1 (TGF-β1) and collagen IV were measured by real time PCR and Western blot. Reactive oxygen species (ROS) production was assessed by fluorescent probe assays. Cell proliferation was analyzed by 5'-bromo-2'-deoxyuridine incorporation assay. Ang II concentration was measured by an enzyme immunoassay. AGT, ACE and AT1 receptor mRNA levels and Ang II concentration were increased in high glucose (HG) -treated MCs, the cell proliferation rate and the production of TGF-β1 and of collagen IV productions were also increased. The NADPH oxidase inhibitor diphenylenechloride iodonium (DPI) was able to reverse the HG-induced RAS activation and the changes in cell proliferation and collagen synthesis. Supplementation of H2S attenuated HG-induced elevations in ROS and RAS activation. Blockade on H2S biosynthesis from cystathione-γ-lyase (CSE) by DL-propargylglycine (PPG) resulted in effects similar to that of HG treatment. In STZ-induced diabetic rats, the changes in RAS were also reversed by H2S supplementation without affecting blood glucose concentration. These data suggested that the decrease in H2S under hyperglycemic condition leads to an imbalance between oxidative and reductive species. The increased oxidative species results in intrarenal RAS activation, which, in turn, contributes to the pathogenesis of renal dysfunction.
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