ArticleDiabetes, obesity & metabolism2026
Defective high-density lipoprotein lipoprotection in type 2 diabetes during acute myocardial infarction is rescued by apolipoprotein M/sphingosine-1-phosphate loading.
Article in Diabetes, obesity & metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- APOM-associated inflammation and apoptosis in stroke-exacerbated myocardial infarction: implications for brain-heart interactions.Apoptosis : an international journal on programmed cell death · 2026Article
- Defective high-density lipoprotein lipoprotection in type 2 diabetes during acute myocardial infarction is rescued by apolipoprotein M/sphingosine-1-phosphate loading.Diabetes, obesity & metabolism · 2026Article
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Authors and funding
13 authors.
Funding
Abstract
aimsMortality of patients with type 2 diabetes (T2D) after acute myocardial infarction (AMI) is tremendous and massively increased compared to non-T2D individuals. The reasons are unclear. High-density lipoprotein (HDL) conducts lipoprotection during AMI, leading to improved outcomes. We hypothesised that T2D-HDL lacks lipoprotective properties. MATERIALS AND
methodsHDL was isolated from healthy, non-T2D individuals and T2D patients. This human HDL was administered to mice undergoing AMI. Infarct size and cardiac function were assessed by histology and echocardiography. HDL composition was determined by mass spectrometry.
resultsHDL from healthy individuals but not from T2D patients reduced infarct size and improved cardiac function after AMI. Analysing HDL composition revealed lack of sphingosine-1-phosphate and Apolipoprotein M in T2D-HDL. Ex-vivo loading of HDL with these components rescued T2D-HDL lipoprotection.
conclusionsWe revealed that T2D-HDL lacks lipoprotection during AMI. This might be a reason for enhanced mortality of T2D patients after AMI. Furthermore, we found an option to rescue T2D-HDL lipoprotection.
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