Key result
Inflammaging and mitochondrial dysfunction drive cardiac aging, leading to structural changes and an increased risk of heart failure with preserved ejection fraction.
This review highlights the role of age-related mitochondrial dysfunction and chronic sterile inflammation in the development of cardiac fibrosis and heart failure with preserved ejection fraction.
Advances in healthcare and improvements in living conditions have led to rising life expectancy worldwide. Aging is associated with excessive oxidative stress, a chronic inflammatory state, and limited tissue healing, all of which result in an increased risk of heart failure. In fact, the prevalence of heart failure approaches 40% in the ninth decade of life, with the majority of these cases suffering from heart failure with preserved ejection fraction (HFpEF). In cardiomyocytes (CMs), age-related mitochondrial dysfunction results in disrupted calcium signaling and covalent protein-linked aggregates, which cause cardiomyocyte functional disturbances, resulting in increased stiffness and diastolic dysfunction. Importantly, aging is also associated with chronic low-grade, sterile inflammation, which alters the function of interstitial cardiac cells and leads to cardiac fibrosis. Taken together, cardiac aging is associated with cellular, structural, and functional changes in the heart that contribute to the rising prevalence of heart failure in older people.
No takes yet. Share an insight, caveat, or question.
Goldstein et al. (2023) conducted a review in Cardiac aging and Heart Failure. Inflammaging and mitochondrial dysfunction was evaluated. Inflammaging and mitochondrial dysfunction drive cardiac aging, leading to structural changes and an increased risk of heart failure with preserved ejection fraction.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: