Roles of Hydrogen Sulfide Donors in Common Kidney Diseases

Ngowi, Ebenezeri Erasto; Sarfraz, Muhammad; Afzal, Attia; Khan, Nazeer Hussain; Khattak, Saadullah; Zhang, Xin; Li, Tao; Duan, Shaofeng; Ji, Xin‐Ying; Wu, Dongdong

doi:10.3389/fphar.2020.564281

Cited by 35 publications

(20 citation statements)

References 201 publications

(336 reference statements)

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“…Previous research also found that endogenous H 2 S supplement ameliorated carbon tetrachloride and high fat diet induced liver fibrosis in rats [11]. H 2 S significantly alleviated renal fibrosis by attenuating collagen accumulation and extracellular matrix remodeling in the kidney of diabetic mice and gentamicin-induced rats [12]. H 2 S also prevented smoke-induced pulmonary fibrosis in rats and alleviated systemic sclerosis associated lung fibrosis in mice [13].…”

Section: Introductionmentioning

confidence: 80%

Necroptosis Inhibition by Hydrogen Sulfide Alleviated Hypoxia-Induced Cardiac Fibroblasts Proliferation via Sirtuin 3

Zhang

Gong

Meng

et al. 2021

IJMS

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Myocardial ischemia or hypoxia can induce myocardial fibroblast proliferation and myocardial fibrosis. Hydrogen sulfide (H2S) is a gasotransmitter with multiple physiological functions. In our present study, primary cardiac fibroblasts were incubated with H2S donor sodium hydrosulfide (NaHS, 50 μM) for 4 h followed by hypoxia stimulation (containing 5% CO2 and 1% O2) for 4 h. Then, the preventive effects on cardiac fibroblast proliferation and the possible mechanisms were investigated. Our results showed that NaHS reduced the cardiac fibroblast number, decreased the hydroxyproline content; inhibited the EdU positive ratio; and down-regulated the expressions of α-smooth muscle actin (α-SMA), the antigen identified by monoclonal antibody Ki67 (Ki67), proliferating cell nuclear antigen (PCNA), collagen I, and collagen III, suggesting that hypoxia-induced cardiac fibroblasts proliferation was suppressed by NaHS. NaHS improved the mitochondrial membrane potential and attenuated oxidative stress, and inhibited dynamin-related protein 1 (DRP1), but enhanced optic atrophy protein 1 (OPA1) expression. NaHS down-regulated receptor interacting protein kinase 1 (RIPK1) and RIPK3 expression, suggesting that necroptosis was alleviated. NaHS increased the sirtuin 3 (SIRT3) expressions in hypoxia-induced cardiac fibroblasts. Moreover, after SIRT3 siRNA transfection, the inhibitory effects on cardiac fibroblast proliferation, oxidative stress, and necroptosis were weakened. In summary, necroptosis inhibition by exogenous H2S alleviated hypoxia-induced cardiac fibroblast proliferation via SIRT3.

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Section: Introductionmentioning

confidence: 80%

Necroptosis Inhibition by Hydrogen Sulfide Alleviated Hypoxia-Induced Cardiac Fibroblasts Proliferation via Sirtuin 3

Zhang

Gong

Meng

et al. 2021

IJMS

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“…In addition, CSE is commonly expressed in endothelial and mesangial cells and podocytes [51]. In kidney diseases, H 2 S ameliorates renal damage [52]. It has been shown that H 2 S attenuates kidney injury during I/R and diabetic kidney disease (DKD).…”

Section: Figurementioning

confidence: 99%

Mitochondrial Redox Signaling and Oxidative Stress in Kidney Diseases

et al. 2021

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Mitochondria are essential organelles in physiology and kidney diseases, because they produce cellular energy required to perform their function. During mitochondrial metabolism, reactive oxygen species (ROS) are produced. ROS function as secondary messengers, inducing redox-sensitive post-translational modifications (PTM) in proteins and activating or deactivating different cell signaling pathways. However, in kidney diseases, ROS overproduction causes oxidative stress (OS), inducing mitochondrial dysfunction and altering its metabolism and dynamics. The latter processes are closely related to changes in the cell redox-sensitive signaling pathways, causing inflammation and apoptosis cell death. Although mitochondrial metabolism, ROS production, and OS have been studied in kidney diseases, the role of redox signaling pathways in mitochondria has not been addressed. This review focuses on altering the metabolism and dynamics of mitochondria through the dysregulation of redox-sensitive signaling pathways in kidney diseases.

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“…Depending on its origin, AKI affects preferentially either glomerular or tubular structures of the kidney. A protective role of hydrogen sulfide in AKI on all kidney segments, including the tubules, is reviewed elsewhere [ 7 , 60 , 61 ]. The effects of AKI in the context of different forms of glomerulonephritis is, so far, poorly understood.…”

Section: The Role Of H 2 S In Glomerular Pathophys...mentioning

confidence: 99%

“…This stress situation interferes with the complex and fine-tuned intraglomerular crosstalk between mesangial cells, glomerular epithelial cells (podocytes) and glomerular endothelial cells resulting in a disturbance of glomerular integrity and function [ 3 , 4 , 5 , 6 ]. In the last decade, the research on H 2 S in animal models revealed promising results for the pharmacological use of H 2 S-releasing drugs for the treatment of glomerular kidney diseases [ 7 ]. Here, we briefly discuss the role of H 2 S in glomerulopathies with a focus on the molecular mechanisms of production and action of this signalling mediator.…”

Section: Introductionmentioning

confidence: 99%

The Pathophysiology of H2S in Renal Glomerular Diseases

Beck

Pfeilschifter

2022

Biomolecules

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Renal glomerular diseases such as glomerulosclerosis and diabetic nephropathy often result in the loss of glomerular function and consequently end-stage renal disease. The glomerulus consists of endothelial cells, mesangial cells and glomerular epithelial cells also referred to as podocytes. A fine-tuned crosstalk between glomerular cells warrants control of growth factor synthesis and of matrix production and degradation, preserving glomerular structure and function. Hydrogen sulfide (H2S) belongs together with nitric oxide (NO) and carbon monoxide (CO) to the group of gasotransmitters. During the last three decades, these higher concentration toxic gases have been found to be produced in mammalian cells in a well-coordinated manner. Recently, it became evident that H2S and the other gasotransmitters share common targets as signalling devices that trigger mainly protective pathways. In several animal models, H2S has been demonstrated as a protective factor in the context of kidney disorders, in particular of diabetic nephropathy. Here, we focus on the synthesis and action of H2S in glomerular cells, its beneficial effects in the glomerulus and its action in the context of the other gaseous signalling molecules NO and CO.

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Roles of Hydrogen Sulfide Donors in Common Kidney Diseases

Cited by 35 publications

References 201 publications

Necroptosis Inhibition by Hydrogen Sulfide Alleviated Hypoxia-Induced Cardiac Fibroblasts Proliferation via Sirtuin 3

Necroptosis Inhibition by Hydrogen Sulfide Alleviated Hypoxia-Induced Cardiac Fibroblasts Proliferation via Sirtuin 3

Mitochondrial Redox Signaling and Oxidative Stress in Kidney Diseases

The Pathophysiology of H2S in Renal Glomerular Diseases

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