Mitochondrial Dysfunction in Cardiac Disease: The Fort Fell

preprint OA: closed CC-BY-4.0
🔓 Open OA copy View at publisher
AI-generated summary by claude@2026-07, 2026-07-17

This review explores how mitochondrial dysfunction, altered energy production and consumption, and subsequent toxic product accumulation contribute to changes in myocardial cell function and cardiac architecture during aging and heart failure.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

Abstract

Myocardial cells and extracellular matrix fulfil their goal thanks to the energetic availability. Indeed, mechanical and electrical properties of the heart are strongly depended on the energetic production-consumption equilibrium. The produced energy is used under several forms including kinetic, dynamic, thermal energy etc. Notably, as the time goes by; aging as well as in case of heart failure, although total energy remains almost constant the contribution of each energetic form is altered. Thermal energy is increased, whereas the dynamic and kinetic energy are decreased and hence unable to satisfy adequately the cardiac work. Consequently, toxic products, unfolded /misfolded proteins, free radicals etc. are accumulated within the myocardium. Myocardial cell contraction – relaxation coupling, ion exchange, cell growth etc. function is failed, control of cell apoptosis and necrosis is lacking and cardiac micro and macro-architecture change is the final result. Energy production and consumption depends on cardiac metabolic resources and on the functional status of the cardiac silhouette including cardiomyocytes and non-cardiomyocytes cells and their metabolic - energetic behavior. Mitochondria, are intra-cellular organelles producing more than 95% of ATP and fulfill all the above prerequisites being thus very important and as such we have to better understand their anatomy, function and homeostatic properties.

My notes (saved in your browser only)

Citation neighborhood (no data yet)

We don't have any in-corpus citations linked to this paper yet. This is a recent paper (2024) — citers typically take a year or two to land, and the OpenAlex reference graph may still be filling in.

Source provenance

europepmc
last seen: 2026-05-20T01:45:00.602351+00:00
unpaywall
last seen: 2026-05-27T02:00:06.600101+00:00
License: CC-BY-4.0