ArticleThe Journal of physiology2003
Depressed mitochondrial transcription factors and oxidative capacity in rat failing cardiac and skeletal muscles.
Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 199 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
199 citing papers in PubMed, 1 synthesis or guideline pooled it, 423 citations in OpenAlex.
- Reprogramming heart failure: physiological orchestration and mechanistic decoding of exercise benefits.BMC cardiovascular disorders · 2025Pooled it
- N-Lac-Phe Ameliorates Myocardial Cell Death by Improving Mitochondrial Dysfunction, Ultimately Improving TAC-induced Heart Failure.Cardiovascular drugs and therapy · 2026Article
- Near-Infrared Spectroscopy in the Pathophysiology, Diagnosis, and Exercise-Based Management of Muscle Oxygenation Impairment.Diagnostics (Basel, Switzerland) · 2026Review
- TIGAR deficiency enhances cardiac resilience through epigenetic programming of Parkin expression.JCI insight · 2026Article
- Structural and Metabolic Remodeling of Skeletal Muscle in Heart Failure with Reduced Ejection Fraction: A Review: Beyond the Failing Heart.International journal of molecular sciences · 2026Review
- A perspective on the future of heart failure research.Journal of molecular and cellular cardiology plus · 2026Article
- Integrated bioinformatic and in vivo analysis confirms the cardioprotective role of OPA1.BMC cardiovascular disorders · 2025Article
- Sex-specific benefits of a combined supplementation of B vitamins, nicotinamide riboside, folate and cobalamin, in a murine model of heart failure.Biology of sex differences · 2025Article
- Precision Medicine: Therapeutically Targeting Mitochondrial Alterations in Heart Failure.JACC. Basic to translational science · 2025Review
- Dissecting the exercise pressor reflex in heart failure: A multi-step failure.Autonomic neuroscience : basic & clinical · 2025Review
- Therapeutic potential of ketone bodies on exercise intolerance in heart failure: looking beyond the heart.Cardiovascular research · 2025Review
- Advances in myocardial energy metabolism: metabolic remodelling in heart failure and beyond.Cardiovascular research · 2024Review
- Mitochondrial Dysfunction as a Potential Mechanism Mediating Cardiac Comorbidities in Parkinson's Disease.International journal of molecular sciences · 2024Review
- SIRT6 in Regulation of Mitochondrial Damage and Associated Cardiac Dysfunctions: A Possible Therapeutic Target for CVDs.Cardiovascular toxicology · 2024Review
- Lipid Toxicity in the Cardiovascular-Kidney-Metabolic Syndrome (CKMS).Biomedicines · 2024Review
- Postnatal growth restriction alters myocardial mitochondrial energetics in mice.Experimental physiology · 2024Article
- Peroxisome proliferator-activated receptor gamma coactivator-1 (PGC-1) family in physiological and pathophysiological process and diseases.Signal transduction and targeted therapy · 2024Review
- Effects of FermentedNutrients · 2024Article
- 3D reconstruction of murine mitochondria reveals changes in structure during aging linked to the MICOS complex.Aging cell · 2023Article
- Recovery from FOLFOX chemotherapy-induced systemic and skeletal muscle metabolic dysfunction in mice.American journal of physiology. Endocrinology and metabolism · 2023Article
139 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Congestive heart failure (CHF) induces alterations in energy metabolism and mitochondrial function that span cardiac as well as skeletal muscles. Whether these defects originate from altered mitochondrial DNA copy number and/or mitochondrial gene transcription is not known at present, nor are the factors that control mitochondrial capacity in different muscle types completely understood. We used an experimental model of CHF induced by aortic banding in the rat and investigated mitochondrial respiration and enzyme activity of biochemical mitochondrial markers in cardiac, slow and fast skeletal muscles. We quantified mitochondrial DNA (mtDNA), expression of nuclear (COX IV) and mitochondrial (COX I) encoded cytochrome c oxidase subunits as well as nuclear factors involved in mitochondrial biogenesis and in the necessary coordinated interplay between nuclear and mitochondrial genomes in health and CHF. CHF induced a decrease in oxidative capacity and mitochondrial enzyme activities with a parallel decrease in the mRNA level of COX I and IV, but no change in mtDNA content. The expression of the peroxisome proliferator activated receptor gamma co-activator 1 alpha (PGC-1 alpha) gene was downregulated in CHF, as well as nuclear respiratory factor 2 and mitochondrial transcription factor A, which act downstream from PGC-1 alpha. Most interestingly, only the level of PGC-1 alpha expression was strongly correlated with muscle oxidative capacity in cardiac and skeletal muscles, both in healthy and CHF rats. Mitochondrial gene transcription is reduced in CHF, and PGC-1 alpha appears as a potential modulator of muscle oxidative capacity under these experimental conditions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.