ReviewJournal of biochemical and molecular toxicology2026
Myocardial Lipid Metabolism Imbalance: The Pathological Core and Novel Diagnostic-Therapeutic Directions of Cardiovascular Diseases.
Review in Journal of biochemical and molecular toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Myocardial Lipid Metabolism Imbalance: The Pathological Core and Novel Diagnostic-Therapeutic Directions of Cardiovascular Diseases.Journal of biochemical and molecular toxicology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Cardiac lipid metabolism is fundamental to myocardial energy homeostasis, with fatty acid oxidation (FAO) supplying the majority of ATP in the healthy adult heart. This review synthesizes the core regulatory network governing cardiac lipid metabolism, encompassing lipid droplet dynamics mediated by perilipins (e.g., Plin5, Plin2), fatty acid uptake via CD36, systemic lipid modulation by apolipoproteins (e.g., APOC3), and the central energy-sensing AMPK/PGC-1α/PPARα axis. Dysregulation of this network initiates a self-perpetuating lipotoxic cycle, characterized by the accumulation of toxic lipid intermediates (e.g., diacylglycerols, ceramides), oxidative stress, and inflammatory activation, which serves as a common pathological mechanism across diverse cardiovascular diseases (CVDs), including atherosclerosis, heart failure, diabetic cardiomyopathy, and ischemic injury. Emerging from this mechanistic understanding is a promising landscape of biomarkers-such as specific ceramide species, the ApoB/ApoA-1 ratio, and circulating perilipins-and targeted therapeutic strategies, including APOC3 inhibitors, SGLT2 inhibitors, and Plin5-directed therapies. Future advances will depend on integrating multi-omics technologies and precision medicine approaches to tailor interventions to specific metabolic phenotypes, thereby opening new avenues for the prevention and treatment of CVDs.
Indexed as
Identifiers
What Socratic 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 Socratic graph.