Actin-Binding Proteins in Cardiac Hypertrophy

Pan, Congbin; Wang, Siqi; Liu, Chao; Ren, Zhanhong

doi:10.3390/cells11223566

Cited by 3 publications

(2 citation statements)

References 116 publications

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“…Previous studies have reported that autophagy; actin-binding proteins, such as cofilin, Formin and capZ; and the MaPK/erK signaling pathway serve roles in cardiac hypertrophy (33)(34)(35). it has been reported that autophagosome formation depends on small GTPases (36).…”

Section: Genementioning

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: Genementioning

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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“…increase the development of cardiac hypertrophy moreover its level is signi cantly increased in mammalian hypertrophic hearts(Kooij et al 2016). On the contrary Pan et al reported that in H9c2 cells the inhibition of pro lin-1 can attenuate cardiac hypertrophy(Pan et al 2022). …”

mentioning

confidence: 96%

Chronic lactate treatment promotes cardiomyocyte cytoskeleton remodelling

Luti,

Militello,

Pinto

et al. 2023

Preprint

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Physical activity is an important regulator of energy homeostasis and helps the improvement of metabolic health lowering the risk for a broad variety of health problems. The driving force of the good health impact of exercise is the new established metabolism in people who practise regular physical activity; in fact, regular physical movement induces a wide variety of molecular adaptations in skeletal muscle and in the whole body. In previous studies performed on elite players, we found that adaptation to exercises is characterized by a chronic high plasma level of lactate. By shuttling between producer and consumer cells, lactate is considered not only an energy source but also a signalling molecule and is referred to as a “lactormone”. In this work, we investigated the effect of exogenous lactate in human cardiomyocyte cell line AC16 assessing their viability, cell cycle activity, oxidative stress and metabolism by a proteomic and metabolomic approach. Interestingly, our data indicated that cardiomyocytes exposed to chronic lactate treatment (72 h) show change in several proteins and metabolites linked to cell hypertrophy and cytoskeleton remodelling.

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