Cardiolipin in Pathology: Implications in Atherosclerosis

Abstract

Mitochondria are cell organelles whose main role is to generate the energy needed for cell biochemical reactions via oxidative phosphorylation. Cardiolipin is a phospholipid that is present in the inner mitochondrial membrane and other energy-transducing membranes. Mitochondrial structure largely depends on cardiolipin, as it is involved in the biogenesis of mitochondrial cristae, folds in the inner mitochondrial membrane designed to increase the surface area, as well as in protein-lipid interactions, oxidative phosphorylation, and other essential processes. Cardiolipin is also substantial for mitochondrial supercomplexes' inner mitochondrial membrane and outer mitochondrial membrane architecture. Changes in cardiolipin profile are able to greatly affect mitochondrial function, leading to its impairment and eventually the development of multiple disorders, such as sterile inflammation, atherosclerosis, metabolic disorders, and neurodegenerative disorders. The role of cardiolipin in the proper functioning of mitochondria ought to be investigated in order to find ways to avert the development of many serious disorders. The aim of this review was to examine available data on the causal connection between cardiolipin alterations and the progression of various pathological conditions, as well as possible ways of preventing these adverse conditions. According to existing literature, alterations in cardiolipin are the potential cause of mitochondrial dysfunction, which stimulates the development of various related disorders. Several therapeutic agents (e.g., elamipretide) have shown promising results in preventing adverse effects of cardiolipin alterations.