ArticleNature communications2025
Inhibiting CD36 palmitoylation improves cardiac function post-infarction by regulating lipid metabolic homeostasis and autophagy.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed.
- TRIM47, stabilized by YTHDF3-mediated m6A modification, promotes cardiac lipid accumulation and aggravates diabetic cardiomyopathy.Molecular metabolism · 2026Article
- Transcriptomic analysis of palmitoylation-related genes reveals a preferential association with BCAA catabolism in adipose tissue from pediatric obesity.Endocrine connections · 2026Article
- Selenotrisulfide delivery restores redox balance in myocardial infarction via a thiol-exchange reactionBioactive materials · 2026Article
- Grx2 deficiency accelerates BMSC senescence and senile osteoporosis via CD36 S-glutathionylation.Cellular & molecular biology letters · 2026Article
- Aptamer-based colorimetric assay on poly(allylamine)-blended polycaprolactone electrospun nanofibers for CD36 detection.Mikrochimica acta · 2026Article
- CD36 as a Context-Dependent Regulator of Metabolic Switching in Acute and Chronic Hypoxia.Biomolecules · 2026Review
- Lipophagy in disease: signaling control, organelle communication, and therapeutic opportunities.Cell communication and signaling : CCS · 2026Review
- Metabolic reprogramming in fibrosis-related diseases: underlying mechanisms and therapeutics.Molecular biomedicine · 2026Review
- Fatty Acid Metabolism in Health and Cancer: From Fundamental Mechanisms to Therapeutic Application.MedComm · 2026Review
- Extracellular Vesicles Modulation by an Adiponectin Receptor Agonist Provides Cardioprotection for Myocardial Ischemic Injury.Advanced healthcare materials · 2026Article
- Cluster of Differentiation 36-Mediated Inflammation and Lipid Metabolism in Cardiovascular Diseases: From Mechanisms to Novel Therapies.Antioxidants (Basel, Switzerland) · 2026Review
- Sigma-1R-CD36 axis in myeloid cells contributes to the alleviation of depression-like behaviors.Journal of translational medicine · 2026Article
- Regulation of mitochondrial fission by Drp1 in cardiomyopathy: possible mechanisms linking cellular processes to cell death.Molecular biology reports · 2026Review
- Targeting the ZDHHC9-mediated STAT1 palmitoylation-phosphorylation conversion inhibits gastric cancer progression.Journal of gastroenterology · 2026Article
- Cardiomyocyte-derived GPX4 stabilizes BNIP3 to facilitate mitophagy and mitigate myocardial ischemia/reperfusion injury.Nature communications · 2026Article
- Loss of miR-146a induces cardiomyocyte proliferation after myocardial infarction through targeting Kctd15.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Endothelial PTBP1 Deletion in Transplanted Cardiac Tissue Limits Cardiac Allograft Vasculopathy.bioRxiv : the preprint server for biology · 2026Article
- Article
- Mechanisms underlying the reversal of hypoxia-induced energy metabolic reprogramming in cardiomyocytes by Poria cocos triterpenoids: integrated regulation of mitochondrial dynamics and the autophagy-lysosomal pathway.Frontiers in cardiovascular medicine · 2026Article
- KIF13B Attenuates Sepsis-Induced Myocardial Dysfunction through the Stabilization of PLIN5.Research (Washington, D.C.) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors.
Funding
Abstract
Alterations in myocardial energy substrate metabolism and mitochondrial injury following myocardial infarction (MI) lead to structural and functional abnormalities of the heart. The fatty acid translocase CD36 (CD36) plays a pivotal role in regulating lipid homeostasis and mitochondrial metabolism. Here, we demonstrate that inhibiting the palmitoylation of CD36 and the resulting alteration in its subcellular localization alleviates lipid metabolism disorders and mitochondrial dysfunction in cardiomyocytes of male mice post-MI. Mechanistically, the inhibition of CD36 palmitoylation enhances cardiac function through a dual mechanism: first, by alleviating fatty acid overload mediated by plasma membrane CD36, thereby restoring lipid metabolic balance; second, by augmenting the activity of the mitochondrial CD36-PGAM5 signaling axis and modulating Fundc1 and Drp1 Dephosphorylation, which subsequently improves mitophagy efficiency. Overall, our study highlights the significant role of CD36 palmitoylation in preserving heart function by regulating downstream metabolic signaling pathways, suggesting that targeting CD36 palmitoylation could be a promising therapeutic strategy for MI.
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.