Mitochondrial Calcium Overload Plays a Causal Role in Oxidative Stress in the Failing Heart.
Biomolecules
; 13(9)2023 09 19.
Article
en En
| MEDLINE
| ID: mdl-37759809
ABSTRACT
Heart failure is a serious global health challenge, affecting more than 6.2 million people in the United States and is projected to reach over 8 million by 2030. Independent of etiology, failing hearts share common features, including defective calcium (Ca2+) handling, mitochondrial Ca2+ overload, and oxidative stress. In cardiomyocytes, Ca2+ not only regulates excitation-contraction coupling, but also mitochondrial metabolism and oxidative stress signaling, thereby controlling the function and actual destiny of the cell. Understanding the mechanisms of mitochondrial Ca2+ uptake and the molecular pathways involved in the regulation of increased mitochondrial Ca2+ influx is an ongoing challenge in order to identify novel therapeutic targets to alleviate the burden of heart failure. In this review, we discuss the mechanisms underlying altered mitochondrial Ca2+ handling in heart failure and the potential therapeutic strategies.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Contexto en salud:
2_ODS3
Problema de salud:
2_cobertura_universal
Asunto principal:
Calcio
/
Insuficiencia Cardíaca
Tipo de estudio:
Prognostic_studies
Límite:
Humans
Idioma:
En
Revista:
Biomolecules
Año:
2023
Tipo del documento:
Article
País de afiliación:
Estados Unidos