Role of Oxidative Stress, Mitochondrial Dysfunction, and Autophagy in Cardiovascular Disease: Its Pathogenesis and Amelioration by Different Small Natural Molecules

Abstract

The biggest cause of global mortality today is cardiovascular diseases. Not only old people, but even the younger generation gets afflicted now. This chapter will focus on the role of oxidative stress, mitochondrial dysfunction, and autophagy on the pathogenesis of the various forms of cardiovascular diseases including heart failure, atherosclerosis, hypertension, myocardial infarction, and ischemia-reperfusion injury. Various cell signaling pathways get modulated under external or internal stress stimuli to induce ROS which begets the oxidative stress condition. The antioxidant defense mechanisms by which the delicate balance between prooxidants and antioxidants in the cell is maintained in equilibrium get disrupted, and the structural and functional entities of the cell collapse. Mitochondrial dysfunction is directly implicated in the above process, as it is both the cause and outcome of oxidative stress. When dysfunctional mitochondria accumulate inside the cell, autophagy comes to the rescue. But excessive autophagy again is a cause of concern as it paves the way for a second type of programmed cell death, distinct from apoptosis. Antioxidants have mostly been proven highly effective against the plethora of cardiovascular diseases, as they have been successful in attenuating the oxidative stress in the vascular cells, as well as that in the myocardial cells, and have restored the physiological conditions close to the normal state. So they have been routed to be important drug leads for the development of effective therapeutics against cardiovascular diseases. With minimal or no toxicity, natural molecules have remained in the forefront to be tested and tried in this regard. So this field has and will continue to have importance in the research fraternity for decades to come.