ArticleFrontiers in physiology2022
Cardiac ischemia modulates white adipose tissue in a depot-specific manner.
Article in Frontiers in physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Cyclic azapeptide CD36 ligand attenuates cardiac injury and reduces long-chain fatty acid accumulation after myocardial ischemia-reperfusion in mice.FEBS open bio · 2026Article
- Comprehensive age-specific metabolic phenotyping in myocardial infarction.BMC cardiovascular disorders · 2026Article
- ATGL From iWAT and BAT Is Crucial for Cardiac Remodeling and Metabolism After Myocardial Ischemia/Reperfusion.Comprehensive Physiology · 2026Article
- SGLT2 inhibition and adipose tissue metabolism: current outlook and perspectives.Cardiovascular diabetology · 2024Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The incidence of heart failure after myocardial infarction (MI) remains high and the underlying causes are incompletely understood. The crosstalk between heart and adipose tissue and stimulated lipolysis has been identified as potential driver of heart failure. Lipolysis is also activated acutely in response to MI. However, the role in the post-ischemic remodeling process and the contribution of different depots of adipose tissue is unclear. Here, we employ a mouse model of 60 min cardiac ischemia and reperfusion (I/R) to monitor morphology, cellular infiltrates and gene expression of visceral and subcutaneous white adipose tissue depots (VAT and SAT) for up to 28 days post ischemia. We found that in SAT but not VAT, adipocyte size gradually decreased over the course of reperfusion and that these changes were associated with upregulation of UCP1 protein, indicating white adipocyte conversion to the so-called 'brown-in-white' phenotype. While this phenomenon is generally associated with beneficial metabolic consequences, its role in the context of MI is unknown. We further measured decreased lipogenesis in SAT together with enhanced infiltration of MAC-2
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