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            S-mediated blockage of protein acetylation and oxidative stress attenuates lipid overload-induced cardiac senescence

Yu, Ruihuan; Wang, Yuehong; Zhu, Jiechun; Yang, Guangdong

doi:10.1080/13813455.2021.1976209

Cited by 8 publications

(4 citation statements)

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“…SREBP1 is a transcription factor that plays a vital role in reducing lipotoxicity by regulating metabolic pathways related to lipogenesis and adipogenesis. The upregulation of ACE2 and the downregulation of SREBP1 in response to lipid overload are indicators of a dysregulated response to lipotoxicity-induced cell injury [22,41]. Another explanation underlying the increased cardiac ACE2 expression by lipid overload could be due the severe oxidative stress, because lipid overload cells had about fivefold of MDA content of the control cells.…”

Section: Discussionmentioning

confidence: 99%

“…H9C2 cells and mouse heart tissues were lysed in 1 mM Tris-EDTA and 0.3 M sucrose buffer (pH 7.2) containing protease inhibitors [21,22]. The protein content of the lysate from cells and tissues was measured using a Pierce bovine serum albumin assay (Fisher Scientific, Toronto, Ontario).…”

Section: Western Blottingmentioning

confidence: 99%

“…For the study with lipid overload, H9C2 cells were incubated with 5 µL/mL of a chemically defined lipid mixture (Sigma-Aldrich, Oakville, ON) for 72 h in the presence or absence of NaHS (30 µM) [22]. The lipid mix contains nonanimal-derived fatty acids (2 μg/mL arachidonic and 10 μg/ mL each linoleic, linolenic, myristic, oleic, palmitic, and stearic), 0.22 mg/mL cholesterol, 2.2 mg/mL Tween-80, 70 μg/mL tocopherol acetate, and 100 mg/mL pluronic F-68.…”

Section: Lipid Overloadmentioning

confidence: 99%

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H2S protects from oxidative stress-driven ACE2 expression and cardiac aging

Barrow

Wang

et al. 2022

Mol Cell Biochem

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Cystathionine gamma-lyase (CSE)-derived hydrogen sulfide (H 2 S) plays an essential role in preserving cardiac functions. Angiotensin-converting enzyme 2 (ACE2) acts as the negative regulator of the renin-angiotensin system, exerting antioxidative stress and anti-inflammatory properties within the body. The interplays of CSE/H 2 S signaling and ACE2 in cardiac aging are unclear. In this study, the regulatory roles of H 2 S on ACE2 expression in mouse heart tissue and rat cardiomyocytes under different stress conditions were investigated. It was found that ACE2 protein level was lower in heart tissues from old mice (56-week-old) than young mice (8-week-old), and the knockout of CSE (CSE KO) induced moderate oxidative stress and further inhibited ACE2 protein level in mouse hearts at both young and old age. Incubation of rat cardiac cells (H9C2) with a low dose of H 2 O 2 (50 µM) suppressed ACE2 protein level and induced cellular senescence, which was completely reversed by co-incubation with 30 µM NaHS (a H 2 S donor). Prolonged nutrient excess is an increased risk of heart disorders by causing metabolic dysfunction and cardiac remodeling. We further found high-fat diet feeding stimulated ACE2 expression and induced severe oxidative stress in CSE KO heart in comparison with wild-type heart. Lipid overload in H9C2 cells to mimic a status of nutrient excess also enhanced the expression of ACE2 protein and induced severe oxidative stress and cell senescence, which were significantly attenuated by the supplementation of exogenous H 2 S. Furthermore, the manipulation of ACE2 expression partially abolished the protective role of H 2 S against cellular senescence. These results demonstrate the dynamic roles of H 2 S in the maintenance of ACE2 levels under different levels of oxidative stress, pointing to the potential implications in targeting the CSE/H 2 S system for the interruption of aging and diabetes-related heart disorders.

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Section: Discussionmentioning

confidence: 99%

Section: Western Blottingmentioning

confidence: 99%

Section: Lipid Overloadmentioning

confidence: 99%

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H2S protects from oxidative stress-driven ACE2 expression and cardiac aging

Barrow

Wang

et al. 2022

Mol Cell Biochem

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“…In the state of WC, the energy demand is excessively high, and the rate of fat deposition is significantly increased, resulting in lipid overload, which is accompanied by lipotoxicity, oxidative stress, and mitochondrial dysfunction [ 116 , 117 ]. In addition, WC significantly reduced adiponectin's expression and increased resistin's expression, suggesting that it may induce metabolic disorders through the dysregulation of adipokine expression [ 118 ]. WC significantly decreased adiponectin expression and increased resistin expression, suggesting that it may induce metabolic disorders through the dysregulation of adipokine expression [ 53 , 104 ].…”

Section: Possible Causes Of Wc: Metaflammation In the Microenvironmen...mentioning

confidence: 99%

Weight cycling based on altered immune microenvironment as a result of metaflammation

Chen

2023

Nutr Metab (Lond)

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As a result of the obesity epidemic, more people are concerned about losing weight; however, weight regain is common, leading to repeated weight loss and weight cycling. The health benefits of early weight loss are nullified by weight regain after weight cycling, which has much more severe metabolic consequences. Weight cycling alters body composition, resulting in faster fat recovery and slower muscle reconstruction. This evident fat accumulation, muscle loss, and ectopic fat deposition destroy the intestinal barrier, increase the permeability of the small intestinal epithelium, and cause the lipotoxicity of lipid metabolites and toxins to leak into extraintestinal tissues and circulation. It causes oxidative stress and hypoxia in local tissues and immune cell infiltration in various tissues, all contributing to the adaptation to this metabolic change. Immune cells transmit inflammatory responses in adipose and skeletal muscle tissue by secreting cytokines and adipokines, which mediate immune cell pathways and cause metaflammation and inefficient metabolic degradation. In this review, we focus on the regulatory function of the immunological microenvironment in the final metabolic outcome, with a particular emphasis on the cellular and molecular processes of local and systemic metaflammation induced by weight cycling-induced changes in body composition. Metaflammation in adipose and muscle tissues that is difficult to relieve may cause weight cycling. As this chronic low-grade inflammation spreads throughout the body, metabolic complications associated with weight cycling are triggered. Inhibiting the onset and progression of metabolic inflammation and enhancing the immune microenvironment of adipose and muscle tissues may be the first step in addressing weight cycling.

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Increased hydrogen sulfide turnover serves a cytoprotective role during the development of replicative senescence

Kieronska-Rudek,

Ascencao,

Chlopicki

et al. 2024

Biochemical Pharmacology

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H ₂ S-mediated blockage of protein acetylation and oxidative stress attenuates lipid overload-induced cardiac senescence

Cited by 8 publications

References 53 publications

H2S protects from oxidative stress-driven ACE2 expression and cardiac aging

H2S protects from oxidative stress-driven ACE2 expression and cardiac aging

Weight cycling based on altered immune microenvironment as a result of metaflammation

Increased hydrogen sulfide turnover serves a cytoprotective role during the development of replicative senescence

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H 2 S-mediated blockage of protein acetylation and oxidative stress attenuates lipid overload-induced cardiac senescence

Cited by 8 publications

References 53 publications

H2S protects from oxidative stress-driven ACE2 expression and cardiac aging

H2S protects from oxidative stress-driven ACE2 expression and cardiac aging

Weight cycling based on altered immune microenvironment as a result of metaflammation

Increased hydrogen sulfide turnover serves a cytoprotective role during the development of replicative senescence

Contact Info

Product

Resources

About

H ₂ S-mediated blockage of protein acetylation and oxidative stress attenuates lipid overload-induced cardiac senescence