Mitochondrial function as a therapeutic target in heart failure
By David A. Brown, Justin B. Perry, Mitchell E. Allen, H. Sabbah, B. Stauffer, S. Shaikh, J. Cleland, W. Colucci, J. Butler, A. Voors and 6 more. Nature Reviews Cardiology, 2016
649 citations recorded by the source corpus.
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.
Subfields: Electrical and Electronic Engineering, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/32a0215b15679aa08e63cb39e144728463487fe9
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Citations in the corpus
- Mitochondrial dysfunction in pathophysiology of heart failure (2018, background): “Prior efforts, primarily focused on reducing oxidative stress and improving bioenergetics, have yielded limited clinical success despite positive results from preclinical studies (38, 39).”
- Mitochondrial dysfunction: mechanisms and advances in therapy (2024, background): “22 Therefore, it ’ s imperative to target mitochondrial dysfunction, given its central role in cardio-cerebrovascular energy depletion and its in fl uence on phenotype enhancement.”