Cardiac hypertrophy, which is characterized by reactivation of certain fetal genes in the heart, increase of sarcomeres, and enlargement of cell size of cardiomyocytes, is a complication and pathological process of many forms of cardiovascular disease, including hypertension, congestive heart failure, valvular diseases and ischemic diseases. Cardiac hypertrophy is initially an adaptive response to pressure or volume overload. The myocardium undergoes hypertrophic growth as a compensatory measure aiming to maintain cardiac output and reduce wall stress. However, increase in mass and volume of myocardial tissue inevitably increase oxygen consumption and dysfunction of energy metabolism in myocardial tissue. The continued presence and evolving hypertrophy eventually lead to decompensation of heart function. Various research have demonstrated that ventricular hypertrophy and remodeling is associated with a significantly increased risk of heart failure, malignant arrhythmia, and even sudden death, and is thought to be an independent risk factor for increasing morbidity and mortality of cardiovascular diseases. Therefore, clinical guidelines in many countries and organizations have suggested it as their primary goal to control and reverse cardiac hypertrophy using therapeutics for hypertension and chronic heart failure.
A variety of neurohumoral factors, receptors, and molecular components in the signaling pathway are involved in the development of cardiac hypertrophy, and complex cross-talk and feedback among them are widely present. Although the molecular mechanisms underlying cardiac hypertrophy have been extensively studied, there remains a large number of unknowns that needs to be further explored thoroughly; especially the mechanisms of transformation from compensation to decompensation. Even though there are some antihypertensive agents that can alleviate cardiac hypertrophy to a certain extent, the effects of these drugs with a single target are limited owing to the compensatory role of other factors.
Therefore in this Research Topic, we aim to provide a platform for researchers and readers to focus on the mechanism of cardiac hypertrophy, remodeling, heart failure, as well as the corresponding intervention drugs.
We encourage investigators to submit to this Research Topic in the form of both Original Research articles and Reviews about the molecular mechanism of cardiac hypertrophy and potential drug effects. Manuscripts involving drug target studies, therapeutic applications, and Clinical Trials are also welcome.
Cardiac hypertrophy, which is characterized by reactivation of certain fetal genes in the heart, increase of sarcomeres, and enlargement of cell size of cardiomyocytes, is a complication and pathological process of many forms of cardiovascular disease, including hypertension, congestive heart failure, valvular diseases and ischemic diseases. Cardiac hypertrophy is initially an adaptive response to pressure or volume overload. The myocardium undergoes hypertrophic growth as a compensatory measure aiming to maintain cardiac output and reduce wall stress. However, increase in mass and volume of myocardial tissue inevitably increase oxygen consumption and dysfunction of energy metabolism in myocardial tissue. The continued presence and evolving hypertrophy eventually lead to decompensation of heart function. Various research have demonstrated that ventricular hypertrophy and remodeling is associated with a significantly increased risk of heart failure, malignant arrhythmia, and even sudden death, and is thought to be an independent risk factor for increasing morbidity and mortality of cardiovascular diseases. Therefore, clinical guidelines in many countries and organizations have suggested it as their primary goal to control and reverse cardiac hypertrophy using therapeutics for hypertension and chronic heart failure.
A variety of neurohumoral factors, receptors, and molecular components in the signaling pathway are involved in the development of cardiac hypertrophy, and complex cross-talk and feedback among them are widely present. Although the molecular mechanisms underlying cardiac hypertrophy have been extensively studied, there remains a large number of unknowns that needs to be further explored thoroughly; especially the mechanisms of transformation from compensation to decompensation. Even though there are some antihypertensive agents that can alleviate cardiac hypertrophy to a certain extent, the effects of these drugs with a single target are limited owing to the compensatory role of other factors.
Therefore in this Research Topic, we aim to provide a platform for researchers and readers to focus on the mechanism of cardiac hypertrophy, remodeling, heart failure, as well as the corresponding intervention drugs.
We encourage investigators to submit to this Research Topic in the form of both Original Research articles and Reviews about the molecular mechanism of cardiac hypertrophy and potential drug effects. Manuscripts involving drug target studies, therapeutic applications, and Clinical Trials are also welcome.
