Related Experiment Videos
Endothelins and cardiac hypertrophy
1Second Department of Internal Medicine, Tokyo Medical & Dental University, Bunkyo-ku, Japan. hito.med2@med.tmd.ac.jp
Insights
Endothelin-1 (ET-1) contributes to cardiac hypertrophy, a common heart condition. This review explores ET-1's roles in heart disease, offering insights into its physiological and pathological functions.
Area of Science:
- Cardiovascular Physiology
- Molecular Cardiology
- Endocrinology
Background:
- Cardiac hypertrophy is a significant complication of cardiovascular diseases.
- Mechanical stress and humoral factors contribute to cardiac hypertrophy.
- Endothelin-1 (ET-1) was identified as a potent inducer of cardiomyocyte hypertrophy in the early 1990s.
Purpose of the Study:
- To review the physiological and pathophysiological roles of endothelin-1 (ET-1) and related peptides.
- To discuss the involvement of ET-1 in cardiac hypertrophy associated with various cardiovascular diseases.
- To consolidate current evidence on ET-1's autocrine/paracrine functions in cardiac hypertrophy.
Main Methods:
- Literature review of studies on endothelin-1 and cardiac hypertrophy.
- Analysis of in vitro and in vivo experimental data.
- Discussion of clinical evidence linking ET-1 to cardiovascular diseases.
Main Results:
- Endothelin-1 (ET-1) induces cardiomyocyte hypertrophy.
- Evidence supports ET-1 acting as an autocrine/paracrine factor in cardiac hypertrophy.
- ET-1 plays roles in various cardiovascular diseases.
Conclusions:
- Endothelin-1 (ET-1) is a key mediator in the development of cardiac hypertrophy.
- Understanding ET-1's roles is crucial for managing cardiovascular diseases.
- Further research into ET-1 pathways may reveal therapeutic targets.
Abstract:
Cardiac hypertrophy is a commonly observed complication of a variety of cardiovascular diseases. As well as mechanical stresses such as pressure overload, several humoral factors may contribute to the development of cardiac hypertrophy. In the early 1990s, endothelin-1 (ET-1) was found to induce cardiomyocyte hypertrophy in cultured neonatal rat cardiomyocytes. Furthermore, evidence is accumulating to date to support the postulate that ET-1 may function as an autocrine/paracrine factor in the development of cardiac hypertrophy in vivo as well as in vitro In this review article, I discuss physiological and pathophysiological roles of ET-1 and its related peptides in cardiac hypertrophy associated with various cardiovascular diseases.