Mitochondrial dysfunction in human hypertrophic cardiomyopathy is linked to cardiomyocyte architecture disruption and corrected by improving NADH-driven mitochondrial respiration.
Edgar E NolletInez DuursmaAnastasiya RozenbaumMoritz EggelbuschRob C I WüstStephan A C SchoonveldeMichelle MichelsMark JansenNicole N van der WelKenneth C BediKenneth B MarguliesJeff NirschlDiederik W D KusterJolanda van der VeldenPublished in: European heart journal (2023)
Mitochondrial dysfunction is explained by cardiomyocyte architecture disruption and is linked to septal hypertrophy in genotype-negative HCM. Despite severe myocardial remodelling mitochondria were responsive to treatments aimed at restoring respiratory function, eliciting the mitochondria as a drug target to prevent and ameliorate cardiac disease in HCM. Mitochondria-targeting therapy may particularly benefit genotype-negative patients with HCM, given the tight link between mitochondrial impairment and septal thickening in this subpopulation.
Keyphrases
- hypertrophic cardiomyopathy
- left ventricular
- cell death
- endoplasmic reticulum
- reactive oxygen species
- oxidative stress
- endothelial cells
- cancer therapy
- heart failure
- angiotensin ii
- blood brain barrier
- high glucose
- induced pluripotent stem cells
- emergency department
- pluripotent stem cells
- adverse drug
- drug induced
- drug delivery
- mesenchymal stem cells
- respiratory tract
- cell therapy
- atrial fibrillation
- electronic health record