7 research outputs found
Quercetin treatment increases H2O2 removal by restoration of endogenous antioxidant activity and blocks isoproterenol-induced cardiac hypertrophy
Limb Blood Flow Restriction Plus Mild Aerobic Exercise Training Protects the Heart Against Isoproterenol-Induced Cardiac Injury in Old Rats: Role of GSK-3β
CaMKII induces permeability transition through Drp1 phosphorylation during chronic β-AR stimulation
Expert consensus document: Mitochondrial function as a therapeutic target in heart failure
Heart failure is a pressing worldwide public-health problem with millions of patients
having worsening heart failure. Despite all the available therapies, the condition carries a very
poor prognosis. Existing therapies provide symptomatic and clinical benefit, but do not fully
address molecular abnormalities that occur in cardiomyocytes. This shortcoming is particularly
important given that most patients with heart failure have viable dysfunctional myocardium,
in which an improvement or normalization of function might be possible. Although the
pathophysiology of heart failure is complex, mitochondrial dysfunction seems to be an important
target for therapy to improve cardiac function directly. Mitochondrial abnormalities include
impaired mitochondrial electron transport chain activity, increased formation of reactive oxygen
species, shifted metabolic substrate utilization, aberrant mitochondrial dynamics, and altered ion
homeostasis. In this Consensus Statement, insights into the mechanisms of mitochondrial
dysfunction in heart failure are presented, along with an overview of emerging treatments
with the potential to improve the function of the failing heart by targeting mitochondria.peerReviewe