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.
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http://dx.doi.org/10.1038/nrcardio.2016.203 | DOI Listing |
Circ Res
January 2025
Hypertension Research Laboratory, School of Biological Sciences (R.R.M., T.Z., E.D., L.X., A.B.-W., H.A.J., M.N., M.P., K.C.L., W.Q., J.A.O.D., F.Z.M.).
Background: Fermentation of dietary fiber by the gut microbiota leads to the production of metabolites called short-chain fatty acids, which lower blood pressure and exert cardioprotective effects. Short-chain fatty acids activate host signaling responses via the functionally redundant receptors GPR41 and GPR43, which are highly expressed by immune cells. Whether and how these receptors protect against hypertension or mediate the cardioprotective effects of dietary fiber remains unknown.
View Article and Find Full Text PDFCirc Genom Precis Med
January 2025
Department of Cardiology, Cardiovascular Research Institute Maastricht, Maastricht University, the Netherlands (S.L.V.M.S., N.J.B., M.F.G.H.M.V., V.P.M.v.E., J.A.J.V.).
Circ Heart Fail
January 2025
Department of Cardiology, Copenhagen University Hospital-Bispebjerg and Frederiksberg, Denmark (S.G., J.H.T., J.J.T.).
Circ Heart Fail
January 2025
S.C. Medicina Generale 1, Medical Center, Ospedale di Circolo and Fondazione Macchi, Department of Internal Medicine, ASST Sette Laghi, Varese, Italy.
Circulation
January 2025
Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN (Y.N.V.R., A.T., M.M.R., B.A.B.).
Background: Plasma NT-proBNP (N-terminal pro-B-type natriuretic peptide) is commonly used to diagnose heart failure with preserved ejection fraction (HFpEF), but its diagnostic performance in the ambulatory/outpatient setting is unknown because previous studies lacked objective reference standards.
Methods: Among patients with chronic dyspnea, diagnosis of HFpEF or noncardiac dyspnea was determined conclusively by exercise catheterization in a derivation cohort (n=414), multicenter validation cohort 1 (n=560), validation cohort 2 (n=207), and a nonobese Japanese validation cohort 3 (n=77). Optimal NT-proBNP cut points for HFpEF rule out (optimizing sensitivity) and rule in (optimizing specificity) were derived and tested, stratified by obesity and atrial fibrillation.
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