AI Article Synopsis

  • Elevated levels of angiotensin II (AngII) cause cardiomyocyte hypertrophy, which is linked to cardiovascular diseases, and current treatments are not very effective at reversing this issue.
  • A study investigates the Japanese Kampo medicine Moku-boi-to (MBT) for its potential to protect against AngII-induced cardiomyocyte hypertrophy and cell death, finding that it improves calcium signaling, reduces reactive oxygen species (ROS), and enhances mitochondrial function.
  • Results suggest that MBT has cardioprotective effects through mechanisms potentially involving the angiotensin receptor, highlighting its promise as a safe and effective treatment for cardiac hypertrophy.

Article Abstract

Cardiomyocyte hypertrophy, induced by elevated levels of angiotensin II (AngII), plays a crucial role in cardiovascular diseases. Current therapeutic approaches aim to regress cardiac hypertrophy but have limited efficacy. Widely used Japanese Kampo medicines are highly safe and potential therapeutic agents. This study aims to explore the impact and mechanisms by which Moku-boi-to (MBT), a Japanese Kampo medicine, exerts its potential cardioprotective benefits against AngII-induced cardiomyocyte hypertrophy, bridging the knowledge gap and contributing to the development of novel therapeutic strategies. By evaluating the effects of six Japanese Kampo medicines with known cardiovascular efficiency on AngII-induced cardiomyocyte hypertrophy and cell death, we identified MBT as a promising candidate. MBT exhibited preventive effects against AngII-induced cardiomyocyte hypertrophy, cell death and demonstrated improvements in intracellular Ca signaling regulation, ROS production, and mitochondrial function. Unexpectedly, experiments combining MBT with the AT receptor antagonist losartan suggested that MBT may target the AT receptor. In an isoproterenol-induced heart failure mouse model, MBT treatment demonstrated significant effects on cardiac function and hypertrophy. These findings highlight the cardioprotective potential of MBT through AT receptor-mediated mechanisms, offering valuable insights into its efficacy in alleviating AngII-induced dysfunction in cardiomyocytes. The study suggests that MBT holds promise as a safe and effective prophylactic agent for cardiac hypertrophy, providing a deeper understanding of its mechanisms for cardioprotection against AngII-induced dysfunction.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10661958PMC
http://dx.doi.org/10.3389/fcell.2023.1264076DOI Listing

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