ReviewGlobal cardiology science & practice2026
Incretin-based therapies and PPARγ agonists as regulators of adipokines-Nrf2 axis in diabetic cardiovascular disease.
Review in Global cardiology science & practice, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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Authors and funding
3 authors.
Funding
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Abstract
Oxidative stress and adipokine imbalance are important contributors to the pathogenesis of diabetic cardiovascular disease. The nuclear factor erythroid 2-related factor 2 (Nrf2) regulates antioxidant defense, while adipokines link metabolism and inflammation. Incretin-based therapies and PPARγ agonists may join on these pathways to provide cardiovascular protection beyond glycemic control. This review aims to investigate the current evidence on how incretin-based agents and PPARγ agonists regulate the adipokine-Nrf2 axis and their impact on cardiovascular outcomes in diabetes. A literature search was performed using PubMed, Google Scholar and Scopus to include reviews, experimental, clinical, and translational studies published in English until November 2025. Evidence indicates that incretin-based agents and PPARγ agonists synergistically activate Nrf2 and inhibit NF-kB signaling, leading to improved oxidative status and favorable adipokine levels. Increased adiponectin and omentin, and suppressed resistin, leptin and TNF-α contribute to reduced inflammation and enhanced vascular and myocardial protection. Collectively, combined activation of incretin and PPARγ pathways modulates the adipokine-Nrf2 axis, offering joined antioxidant and anti-inflammatory benefits that may reduce diabetic cardiovascular risk.
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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.