ReviewiScience2026
Integrative insights into fatty acid metabolism in diabetic cardiomyopathy: From molecular mechanisms to therapeutic strategies.
Review in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Molecular Basis of Adipose-Cardiac Crosstalk in Cardiovascular Diseases: From Mechanisms to Therapeutic Opportunities.Biomolecules · 2026Review
- Rewiring Lipid Metabolism: PINK1 as a Central Regulator of Mitochondrial Homeostasis in Parkinson's Disease.International journal of molecular sciences · 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
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic cardiomyopathy (DCM) is a diabetes-specific cardiac dysfunction independent of other cardiovascular diseases. Recent studies highlight dysregulated fatty acid (FA) metabolism as a central driver of its pathogenesis. In the diabetic heart, excessive FA uptake and oxidation imbalance with glucose utilization led to lipid accumulation, mitochondrial overload, and oxidative stress. These changes trigger inflammatory responses, impair mitochondrial structural integrity and quality control, and disrupt cellular energy homeostasis. Over time, this maladaptation promotes cardiomyocyte hypertrophy, interstitial fibrosis, and progressive diastolic dysfunction. This review synthesizes current knowledge on the links between FA metabolic dysregulation and DCM, from metabolic overload to structural remodeling. It also discusses emerging therapeutic strategies aimed at reducing pathological lipid influx, optimizing energy substrate balance, restoring mitochondrial function, and preventing downstream injury, with the goal of guiding precision interventions for DCM.
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.