Title:Novel Molecules Targeting Metabolism and Mitochondrial Function in Cardiac Diseases
Volume: 22
Issue: 1
Author(s): Samir Bolivar Gonzalez, Cesar Vásquez Trincado, Karen Patricia Torres Rodriguez, Lizeth Paola Forero Acosta, Maria Fernanda Perez Garcia, Steffy Saavedra-Castro, Sara Camila Castiblanco-Arroyave, Gerardo Manríquez Higuera, Luis Antonio Diaz-Ariza, Hector Rodriguez Ortiz and Evelyn Mendoza-Torres*
Affiliation:
- Faculty of Health, Exact and Natural Sciences, Universidad Libre Seccional Barranquilla,
Barranquilla, Colombia
Keywords:
Cardiovascular disease, mitochondrial dynamics, heart failure, ischemia, cardiac hypertrophy, metformin, angiotensins, nicotinamide riboside.
Abstract: Cardiovascular diseases (CVD) are the leading cause of death worldwide, creating the
need for new therapeutic strategies targeting the pathological processes involved. Mitochondria,
which comprise one-third of cardiac cell volume, maybe a potential therapeutic target for CVD.
Known primarily for energy production, mitochondria are also involved in other processes including
intermediary metabolism, mitophagy, calcium homeostasis, and regulation of cell apoptosis.
Mitochondrial function is closely linked to morphology, which is altered through mitochondrial
dynamics, including processes such as fission and fusion, which ensure that the energy needs of
the cell are met. Recent data indicate that mitochondrial dysfunction is involved in the pathophysiology
of several CVDs, including cardiac hypertrophy, heart failure, ischemia/reperfusion injury,
and cardiac fibrosis. Furthermore, mitochondrial dysfunction is associated with oxidative stress
related to atherosclerosis, hypertension, and pulmonary hypertension. In this review, we first
briefly present the physiological mechanisms of mitochondrial function in the heart and then
summarize the current knowledge on the impact of mitochondrial dysfunction on CVD. And finally,
we highlight the evidence from in vitro, in vivo, and clinical studies of the cardioprotective effects
of drugs that preserve mitochondrial function in CVD. It is hoped that this review may provide
new insights into the need to discover new pharmacological targets with direct actions on mitochondria
that may provide combined therapeutic strategies to optimally treat these pathologies.
