Myocardial Recovery versus Myocardial Regeneration: Mechanisms and Therapeutic Modulation.

Myocardial recovery is characterized by a return toward normal structure and function of the heart after an injury. Mechanisms of myocardial recovery include restoration and/or adaptation of myocyte structure and function, mitochondrial activity and number, metabolic homeostasis, electrophysiological stability, extracellular matrix remodeling, and myocardial perfusion. Myocardial regeneration is an element of myocardial recovery that involves the generation of new myocardial tissue, a process which is limited in adult humans but may be therapeutically augmented.

Mitochondrial Ca Uniporter-Dependent Energetic Dysfunction Drives Hypertrophy in Heart Failure.

The role of the mitochondrial calcium uniporter (MCU) in energy dysfunction and hypertrophy in heart failure (HF) remains unknown. In angiotensin II (ANGII)-induced hypertrophic cardiac cells we have shown that hypertrophic cells overexpress MCU and present bioenergetic dysfunction. However, by silencing MCU, cell hypertrophy and mitochondrial dysfunction are prevented by blocking mitochondrial calcium overload, increase mitochondrial reactive oxygen species, and activation of nuclear factor kappa B-dependent hypertrophic and proinflammatory signaling.

Future Impact of mRNA Therapy on Cardiovascular Diseases.

The silver lining of the recent pandemic was that it accelerated the emergence of messenger ribonucleic acid (mRNA) therapeutics. The great promise of mRNA therapeutics was highlighted by the speed at which the vaccines were created, tested, and proven to be relatively safe and highly effective. There are a wide variety of mRNA therapeutics now under development, and dozens of these are in clinical trials.