ReviewTrends in endocrinology and metabolism: TEM2020
Metabolism, Epigenetics, and Causal Inference in Heart Failure.
Review in Trends in endocrinology and metabolism: TEM, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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
31 citing papers in PubMed, 40 citations in OpenAlex.
- Bioadaptive spatiotemporal nanomedicine promotes metabolic recovery after myocardial infarction through NADNature cardiovascular research · 2026Article
- Mitochondria‑endoplasmic reticulum contact site nexus: Molecular integration, disease pathogenesis and therapeutic opportunities (Review).International journal of molecular medicine · 2026Review
- The Metabolic Role of Mitochondria in the Perinatal Cardiac Development and Cardiovascular Diseases.Exploration (Beijing, China) · 2026Review
- Review
- Mapping DNA methylation to cardiac pathologies induced by beta-adrenergic stimulation in a large panel of mice.Epigenetics · 2025Article
- Epigenetic Control of Cardiomyocyte Necrosis: Targeting ACSS2 to Attenuate Myocardial Ischemia/Reperfusion Injury.Journal of cardiovascular translational research · 2025Article
- O-GlcNAcylation promotes angiogenic transdifferentiation to reverse vascular ischemia.Nature cardiovascular research · 2025Article
- Unraveling the metabolic‒epigenetic nexus: a new frontier in cardiovascular disease treatment.Cell death & disease · 2025Review
- Mitochondrial Dysfunction in Cardiac Disease: The Fort Fell.Biomolecules · 2024Review
- Sacubitril/valsartan ameliorates cardiac function and ventricular remodeling in CHF rats via the inhibition of the tryptophan/kynurenine metabolism and inflammation.Scientific reports · 2024Article
- Comparative Metabolomics in Single Ventricle Patients after Fontan Palliation: A Strong Case for a Targeted Metabolic Therapy.Metabolites · 2023Review
- Cardiac fibroblasts and mechanosensation in heart development, health and disease.Nature reviews. Cardiology · 2023Review
- Circulating metabolic signatures of heart failure in precision cardiology.Precision clinical medicine · 2023Review
- The Current Therapeutic Role of Chromatin Remodeling for the Prognosis and Treatment of Heart Failure.Biomedicines · 2023Review
- Mitochondria-associated endoplasmic reticulum membranes (MAMs): Possible therapeutic targets in heart failure.Frontiers in cardiovascular medicine · 2023Review
- Cardio-Oncology: Mechanisms, Drug Combinations, and Reverse Cardio-Oncology.International journal of molecular sciences · 2022Review
- DNMT3B System Dysregulation Contributes to the Hypomethylated State in Ischaemic Human Hearts.Biomedicines · 2022Article
- Article
- Cardiovascular informatics: building a bridge to data harmony.Cardiovascular research · 2022Review
- Metabolic remodeling in takotsubo syndrome.Frontiers in cardiovascular medicine · 2022Review
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
Eukaryotes must balance the metabolic and cell death actions of mitochondria via control of gene expression and cell fate by chromatin, thereby functionally binding the metabolome and epigenome. This interaction has far-reaching implications for chronic diseases in humans, the most common of which are those of the cardiovascular system. The most devastating consequence of cardiovascular disease, heart failure, is not a single disease, diagnosis, or endpoint. Human and animal studies have revealed that, regardless of etiology and symptoms, heart failure is universally associated with abnormal metabolism and gene expression - to frame this as cause or consequence, however, may be to wrongfoot the question. This essay aims to challenge current thinking on metabolic-epigenetic crosstalk in heart failure, presenting hypotheses for how chronic diseases arise, take hold, and persist. We unpack assumptions about the order of operations for gene expression and metabolism, exploring recent findings in noncardiac systems that link metabolic intermediates directly to chromatin remodeling. Lastly, we discuss potential mechanisms by which chromatin may serve as a substrate for metabolic memory, and how changes in cellular transcriptomes (and hence in cellular behavior) in response to stress correspond to global changes in chromatin accessibility and structure.
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.