Emerging mitochondrial signaling mechanisms in cardio-oncology: beyond oxidative stress. Am J Physiol Heart Circ Physiol 2022 Oct 01;323(4):H702-H720
Date
08/06/2022Pubmed ID
35930448Pubmed Central ID
PMC9529263DOI
10.1152/ajpheart.00231.2022Scopus ID
2-s2.0-85139374997 (requires institutional sign-in at Scopus site) 10 CitationsAbstract
Many anticancer therapies (CTx) have cardiotoxic side effects that limit their therapeutic potential and cause long-term cardiovascular complications in cancer survivors. This has given rise to the field of cardio-oncology, which recognizes the need for basic, translational, and clinical research focused on understanding the complex signaling events that drive CTx-induced cardiovascular toxicity. Several CTx agents cause mitochondrial damage in the form of mitochondrial DNA deletions, mutations, and suppression of respiratory function and ATP production. In this review, we provide a brief overview of the cardiovascular complications of clinically used CTx agents and discuss current knowledge of local and systemic secondary signaling events that arise in response to mitochondrial stress/damage. Mitochondrial oxidative stress has long been recognized as a contributor to CTx-induced cardiotoxicity; thus, we focus on emerging roles for mitochondria in epigenetic regulation, innate immunity, and signaling via noncoding RNAs and mitochondrial hormones. Because data exploring mitochondrial secondary signaling in the context of cardio-oncology are limited, we also draw upon clinical and preclinical studies, which have examined these pathways in other relevant pathologies.
Author List
Bikomeye JC, Terwoord JD, Santos JH, Beyer AMAuthor
Andreas M. Beyer PhD Associate Professor in the Medicine department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
Adenosine TriphosphateAntineoplastic Agents
Cardiotoxicity
DNA, Mitochondrial
Epigenesis, Genetic
Heart Diseases
Hormones
Humans
Neoplasms
Oxidative Stress
