ArticleAging2025
Multi-omics analysis reveals metabolic disruptions in cardiac tissues of aging nonhuman primates with spontaneous type 2 diabetes.
Article in Aging, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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Who cites it
3 citing papers in PubMed.
- NOR-1 as a Context-Dependent Rheostat of Vascular and Cardiac Remodeling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Targeting Arterial Dysfunction in Cardiovascular Disease Using Stem Cell-Based Therapies.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- The heart of diabetes: unraveling metabolic drivers of cardiomyopathy.Cardiovascular diabetology. Endocrinology reports · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe complex interplay between type 2 diabetes (TM) and obesity, particularly in aging populations, is increasingly recognized for its significant contribution to cardiac dysfunction. However, the metabolic changes within cardiac tissues that underlie this relationship remain poorly understood.
methodsWe employed a multi-omics approach to investigate the metabolic alterations in cardiac tissues of aging nonhuman primates with spontaneous TM and obesity. Comprehensive analysis was conducted on left ventricular heart tissues from control (CON), obesity (OB), and TM groups, each comprising three aging monkeys. Proteomic data were analyzed using label-free mass spectrometry, and lipidomic profiles were determined using targeted metabolomic assays.
resultsOur analysis uncovered significant metabolic perturbations in both the OB and TM groups relative to controls. Notably, the TM group showed alterations in cardiac metal ion metabolic proteins and a disruption in the liver-heart crosstalk, suggesting a derailment in the heart's metabolic support system. This was further exacerbated by reduced levels of short-chain acylcarnitines and lysophosphatidylcholines (lysoPCs), coupled with an increase in C18:2 acylcarnitines. A progressive decline in amino acid levels was observed from the control to OB to TM groups, indicating a stepwise deterioration in cardiac metabolic remodeling.
conclusionsThis multi-omics study in aging nonhuman primates provides novel insights into the metabolic dysregulations associated with TM and obesity in cardiac tissues. The observed metabolic changes highlight potential therapeutic targets for prevention or mitigating the cardiac complications of TM.
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