The Part Mitochondrial Dysfunction Plays in Heart Disease

Abstract

Cardiovascular diseases (CVDs) continue to be the world's largest cause of mortality, even with improvements in diagnosis and care. There is mounting evidence that mitochondrial dysfunction plays a key role in the onset and advancement of CVDs. Because they are involved in the oxidative phosphorylation (OXPHOS) process that produces ATP, mitochondria, also referred to as the powerhouses of the cell, are essential for heart function. Additionally, they control vital cellular functions such redox signaling, calcium balance, and programmed cell death. Heart disease and cellular damage result when mitochondria are unable to maintain these essential functions, which can be caused by oxidative stress, genetic abnormalities, or imbalances in mitochondrial dynamics. Excessive formation of reactive oxygen species (ROS), which lead to oxidative stress and harm cellular components, including mitochondrial DNA (mtDNA), is one of the most harmful effects of mitochondrial malfunction. These alterations impair mitochondrial energy production and set off a vicious cycle of increased ROS buildup and cellular damage.  Furthermore, malfunctions in the mechanisms that regulate mitochondrial quality, including fission, fusion, and mitophagy, make it more difficult for damaged organelles to be eliminated, which results in energy shortages and cardiomyocyte mortality. Increased oxidative damage and accelerated cardiac damage are caused by dysregulated ROS scavenging mechanisms, such as deficits in MnSOD, GPx1, or Trx2. Targeting mitochondrial pathways offers an interesting prospect for new treatment approaches as our knowledge of the heart's mitochondrial function grows. Restoring mitochondrial function, strengthening antioxidant defense, or adjusting mitochondrial dynamics are some interventions that may provide potential ways to lessen the burden of CVD.