Role of mitochondrial homeostasis in D-galactose-induced cardiovascular ageing from bench to bedside.

• A major contributor to cardiovascular ageing is mitochondrial dysfunction. • Cardiovascular ageing characteristics, including diastolic dysfunction, fibrosis, and heart hypertrophy, are facilitated by these alterations. • The D-galactose (D-gal)-induced aging model modulates the multiple mechanisms to facilitate the cardiovascular ageing process. • Treatment with D-galactose causes oxidative stress in the mitochondria and reduces bioenergetics. • Mitochondrial homeostasis mechanism plays a vital role in the cardiovascular ageing process. • To treat or prevent cardiovascular ageing, focusing on mitochondrial dysfunction shows promising result. Ageing is an inevitable phenomenon which affects the cellular to the organism level in the progression of the time. Oxidative stress and inflammation are now widely regarded as the key processes involved in the aging process, which may then cause significant harm to mitochondrial DNA, leading to apoptosis. Normal circulatory function is a significant predictor of disease-free life expectancy. Indeed, disorders affecting the cardiovascular system, which are becoming more common, are the primary cause of worldwide morbidity, disability, and mortality. Cardiovascular aging may precede or possibly underpin overall, age-related health decline. Numerous studies have found mitochondrial mechanistc approach plays a vital role in the in the onset and development of aging. The D-galactose (D-gal)-induced aging model is well recognized and commonly used in the aging study. In this review we redeposit the association of the previous and current studies on mitochondrial homeostasis and its underlying mechanisms in D-galactose cardiovascular ageing. Further we focus the novel and the treatment strategies to combat the major complication leading to the cardiovascular ageing. [ABSTRACT FROM AUTHOR]