ReviewCardiovascular research2010
Mitochondria in heart failure.
Review in Cardiovascular research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
128 citing papers in PubMed, 1 synthesis or guideline pooled it, 236 citations in OpenAlex.
- Reprogramming heart failure: physiological orchestration and mechanistic decoding of exercise benefits.BMC cardiovascular disorders · 2025Pooled it
- Unveiling cellular mechanisms underlying MYZAP related dilated cardiomyopathy using patient specific hiPSC cardiomyocytes.Scientific reports · 2026Article
- Unveiling the importance of SIRT5 for cardiac health and disease in an era of increasing longevity.GeroScience · 2026Review
- Artificial intelligence-driven design and optimization of mitochondria-targeted nanocarriers for chronic heart failure.Frontiers in bioengineering and biotechnology · 2026Review
- Integrative transcriptomic and single-cell analysis reveals mitochondrial-related gene biomarkers in heart failure with preserved ejection fraction.Scientific reports · 2025Article
- Article
- Emerging trends in cardiovascular diseases: the impact of ferroptosis and cuproptosis on cardiomyocyte death.Molecular and cellular biochemistry · 2025Review
- Multi-omics analysis of diabetic cardiomyopathy pathogenesis using a type 2 diabetic Zucker diabetic fatty rat model.Scientific reports · 2025Article
- Alterations in Mitochondrial Function in Pulmonary Vascular Diseases.Antioxidants & redox signaling · 2025Article
- The crosstalk between mitochondrial dysfunction and fatty acid metabolism in heart failure: mechanisms and therapeutic strategies.Frontiers in pharmacology · 2025Review
- Mitochondrial dysfunction in long COVID: mechanisms, consequences, and potential therapeutic approaches.GeroScience · 2024Review
- Food therapy of scutellarein ameliorates pirarubicin‑induced cardiotoxicity in rats by inhibiting apoptosis and ferroptosis through regulation of NOX2‑induced oxidative stress.Molecular medicine reports · 2024Article
- Ironing out the details: ferroptosis and its relevance to diabetic cardiomyopathy.American journal of physiology. Regulatory, integrative and comparative physiology · 2023Review
- Status of Mitochondrial Oxidative Phosphorylation during the Development of Heart Failure.Antioxidants (Basel, Switzerland) · 2023Review
- Decoding molecular signature on heart of septic mice with distinct left ventricular ejection fraction.iScience · 2023Article
- Subcellular omics: a new frontier pushing the limits of resolution, complexity and throughput.Nature methods · 2023Article
- Impact of blood factors on endothelial cell metabolism and function in two diverse heart failure models.PloS one · 2023Article
- Sodium-glucose Cotransporter 2 Inhibitors and Pathological Myocardial Hypertrophy.Current drug targets · 2023Article
- Targeting MCL-1 protein to treat cancer: opportunities and challenges.Frontiers in oncology · 2023Review
- Cuproptosis, the novel therapeutic mechanism for heart failure: a narrative review.Cardiovascular diagnosis and therapy · 2022Review
68 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
2 authors at 1 institution in 1 country.
Funding
Abstract
This review focuses on the evidence accumulated in humans and animal models to the effect that mitochondria are key players in the progression of heart failure (HF). Mitochondria are the primary source of energy in the form of adenosine triphosphate that fuels the contractile apparatus, and are thus essential for the pumping activity of the heart. We evaluate changes in mitochondrial morphology and alterations in the main components of mitochondrial energetics, such as substrate utilization and oxidative phosphorylation coupled with the level of respirasomes, in the context of their contribution to the chronic energy deficit and mechanical dysfunction in HF.
Indexed as
Identifiers
What OpenQuestion holds
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.