Hydrochlorothiazide Reduces Cardiac Hypertrophy, Fibrosis and Rho-Kinase Activation in DOCA-Salt Induced Hypertension

Mondaca‐Ruff, David; Araos, Patricio; Yáñez, Cristian; Novoa, Ulises; Mora, Italo; Ocaranza, María Paz; Jalil, Jorge

doi:10.1177/10742484211053109

Cited by 4 publications

(2 citation statements)

References 65 publications

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“…Likewise, the abnormal upregulation of Rho GTPase functions can induce cardiac hypertrophy. Fasudil, an inhibitor of ROCK, which is a RhoA effector, can inhibit cardiac remodeling and hypertrophy ( 39 ). In addition, vitamin D can inhibit the expression of Rac1 and alleviate pressure overload-induced cardiac hypertrophy ( 40 ), and statins can relieve cardiac hypertrophy by inhibiting Rac1-mediated oxidative stress ( 41 ).…”

Section: Discussionmentioning

confidence: 99%

RICH1 is a novel key suppressor of isoproterenol‑ or angiotensin II‑induced cardiomyocyte hypertrophy

Wang,

Ling

et al. 2024

Mol Med Rep

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Cardiac hypertrophy is one of the key processes in the development of heart failure. Notably, small GTPases and GTPase-activating proteins (GAPs) serve essential roles in cardiac hypertrophy. RhoGAP interacting with CIP4 homologs protein 1 (RICH1) is a RhoGAP that can regulate Cdc42/Rac1 and F-actin dynamics. RICH1 is involved in cell proliferation and adhesion; however, to the best of our knowledge, its role in cardiac hypertrophy remains unknown. In the present study, the role of RICH1 in cardiomyocyte hypertrophy was assessed. Cell viability was analyzed using the Cell Counting Kit-8 assay and cells surface area (CSA) was determined by cell fluorescence staining. Reverse transcription-quantitative PCR and western blotting were used to assess the mRNA expression levels of hypertrophic marker genes, such as Nppa, Nppb and Myh7 , and the protein expression levels of RICH1, respectively. RICH1 was shown to be downregulated in isoproterenol (ISO)- or angiotensin II (Ang II)-treated H9c2 cells. Notably, overexpression of RICH1 attenuated the upregulation of hypertrophy-related markers, such as Nppa, Nppb and Myh7 , and the enlargement of CSA induced by ISO and Ang II. By contrast, the knockdown of RICH1 exacerbated these effects. These findings suggested that RICH1 may be a novel suppressor of ISO- or Ang II-induced cardiomyocyte hypertrophy. The results of the present study will be beneficial to further studies assessing the role of RICH1 and its downstream molecules in inhibiting cardiac hypertrophy.

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Section: Discussionmentioning

confidence: 99%

RICH1 is a novel key suppressor of isoproterenol‑ or angiotensin II‑induced cardiomyocyte hypertrophy

Wang,

Ling

et al. 2024

Mol Med Rep

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“…ჩვენს მიერ ჩატარებული კვლევით მიღებული შედეგები, გარკვეულწილად თანხვედრაშია სხვა მკვლევრების მიერ მიღებულ შედეგებთან [16,17]…”

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Influence of Sacubitril/Valsartan Combination on Cardiac Histomorphological and Morphometric Changes

GOLOSHVILI,

OKUJAVA,

BURJANADZE

et al. 2023

jecm

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Arterial hypertension is one of the most common disease worldwide, which remains the main risk factor for complications of cardiovascular diseases. As it is already known, arterial hypertension affects many organs and organ systems, including the cardiovascular system. Therefore, it is important to start treatment at an early stage of its development and remove the influence on heart remodeling.The study was carried out on 40 male Wistar rats weighing 250.0-300.0g. Animals were randomly divided into the following groups: I -control group (n=10); II -experimental, DOCA (deoxycorticosterone acetate) saline group, for 28 days, to create arterial hypertension, 25 mg/kg DOCA was injected intraperitoneally and animals were given only saline solution (1% NaCl and 0.2% KCl) to drink (n=10); III -treated group. After the development of arterial hypertension (25 mg/kg DOCA and drinking saline solution (1% NaCl and 0.2% KCl)), 30 mg/kg sacubitril-valsartan combination was administered by intraperitoneal injection for 2 weeks (n=10); IV -preventive group. intraperitoneally 25 mg/kg DOCA + 1% NaCl and 0.2% KCl in drinking water + 30 mg/kg sacubitril-valsartan combination for 2 weeks, (n=10);As a result of the study, in the control group, focal moderate blood flow and transverse arrangement of cardiomyocytes were revealed, associated with hypertrophy of cardiomyocytes in the anterior wall of the ventricle in hypertension and fibrosis of the perivascular space compared to the control; Preservation of striations in the post-treatment period, with loss of architecture of fiber structures and wavy structure. In the case of prevention, compared to the control and hypertension groups, the preservation of striation was predominantly manifested.Based on the obtained results, the sacubitril-valsartan combination inhibits the development of cardiac remodeling during its preventive use in the process of formation of arterial hypertension.

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Adult hypertensive rats are more prone to gut microflora perturbation and fibrosis in response to moderate restraint stress

Wang

Gao

et al. 2023

Translational Research

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Hydrochlorothiazide Reduces Cardiac Hypertrophy, Fibrosis and Rho-Kinase Activation in DOCA-Salt Induced Hypertension

Cited by 4 publications

References 65 publications

RICH1 is a novel key suppressor of isoproterenol‑ or angiotensin II‑induced cardiomyocyte hypertrophy

RICH1 is a novel key suppressor of isoproterenol‑ or angiotensin II‑induced cardiomyocyte hypertrophy

Influence of Sacubitril/Valsartan Combination on Cardiac Histomorphological and Morphometric Changes

Adult hypertensive rats are more prone to gut microflora perturbation and fibrosis in response to moderate restraint stress

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