ArticleMetabolism: clinical and experimental2014
Dipeptidyl peptidase inhibition prevents diastolic dysfunction and reduces myocardial fibrosis in a mouse model of Western diet induced obesity.
Article in Metabolism: clinical and experimental, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.
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Who cites it
60 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.
- Incretin-based agents in type 2 diabetic patients at cardiovascular risk: compare the effect of GLP-1 agonists and DPP-4 inhibitors on cardiovascular and pancreatic outcomes.Cardiovascular diabetology · 2017Pooled it
- DPP-4 inhibitor linagliptin modulates myocardial metabolism in a model of coronary artery disease.JTCVS open · 2025Article
- Elimination of hepatocyte-derived DPP4 downregulates cardiac immune- and collagen-related genes but does not alter cardiac function in aged male mice.Physiological reports · 2025Article
- Global research trends on DPP-4 inhibitors and cardiovascular outcomes: a comprehensive bibliometric analysis.Annals of medicine and surgery (2012) · 2025Review
- Functional Roles of CD26/DPP4 in Bleomycin-Induced Pulmonary Hypertension Associated with Interstitial Lung Disease.International journal of molecular sciences · 2024Article
- Comparative effects of canagliflozin and sitagliptin in chronically ischemic myocardium.Vessel plus · 2024Article
- An Overview of the Cardioprotective Effects of Novel Antidiabetic Classes: Focus on Inflammation, Oxidative Stress, and Fibrosis.International journal of molecular sciences · 2023Review
- Gut Molecules in Cardiometabolic Diseases: The Mechanisms behind the Story.International journal of molecular sciences · 2023Review
- Beneficial Effects of Dipeptidyl Peptidase-4 Inhibitors on Heart Failure With Preserved Ejection Fraction and Diabetes.JACC. Asia · 2023Article
- EGCG Alleviates Obesity-Induced Myocardial Fibrosis in Rats by Enhancing Expression of SCN5A.Frontiers in cardiovascular medicine · 2022Article
- Emerging therapies: The potential roles SGLT2 inhibitors, GLP1 agonists, and ARNI therapy for ARNI pulmonary hypertension.Pulmonary circulation · 2022Review
- Heart failure with preserved ejection fraction in humans and mice: embracing clinical complexity in mouse models.European heart journal · 2021Review
- Fibrosis of the diabetic heart: Clinical significance, molecular mechanisms, and therapeutic opportunities.Advanced drug delivery reviews · 2021Review
- Role of novel biomarkers in diabetic cardiomyopathy.World journal of diabetes · 2021Review
- Therapeutic potential of targeting oxidative stress in diabetic cardiomyopathy.Free radical biology & medicine · 2021Review
- Diabetic fibrosis.Biochimica et biophysica acta. Molecular basis of disease · 2021Review
- Roles and Mechanisms of Dipeptidyl Peptidase 4 Inhibitors in Vascular Aging.Frontiers in endocrinology · 2021Review
- Dipeptidyl peptidase 4 inhibitors and their potential immune modulatory functions.Pharmacology & therapeutics · 2020Review
- Astragaloside IV promotes the eNOS/NO/cGMP pathway and improves left ventricular diastolic function in rats with metabolic syndrome.The Journal of international medical research · 2020Article
- Cellular Protein Quality Control in Diabetic Cardiomyopathy: From Bench to Bedside.Frontiers in cardiovascular medicine · 2020Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveConsumption of a high-fat/high-fructose Western diet (WD) is linked to rising obesity and heart disease, particularly diastolic dysfunction which characterizes early obesity/metabolic cardiomyopathy. Mounting evidence supports a role for inflammation, oxidative stress and fibrosis in the pathophysiology of metabolic cardiomyopathy. Dipeptidyl peptidase-4 (DPP-4) is a circulating exopeptidase recently reported to be elevated in the plasma of patients with insulin resistance (IR), obesity and heart failure. We hypothesized that a model of WD induced obesity/metabolic cardiomyopathy would exhibit increased DPP-4 activity and cardiac fibrosis with DPP-4 inhibition preventing cardiac fibrosis and the associated diastolic dysfunction. MATERIALS/
methodsFour-week-old C57BL6/J mice were fed a high-fat/high-fructose WD with the DPP-4 inhibitor MK0626 for 16 weeks. Cardiac function was examined by high-resolution cine-cardiac magnetic resonance imaging (MRI). Phenotypic analysis included measurements of body and heart weight, systemic IR and DPP-4 activity. Immunohistochemistry and transmission electron microscopy (TEM) were utilized to identify underlying pathologic mechanisms.
resultsWe found that chronic WD consumption caused obesity, IR, elevated plasma DPP-4 activity, heart enlargement and diastolic dysfunction. DPP-4 inhibition with MK0626 in WD fed mice resulted in >75% reduction in plasma DPP-4 activity, improved IR and normalized diastolic relaxation. WD consumption induced myocardial oxidant stress and fibrosis with amelioration by MK0626. TEM of hearts from WD fed mice revealed abnormal mitochondrial and perivascular ultrastructure partially corrected by MK0626.
conclusionsThis study provides evidence of a role for increased DPP-4 activity in metabolic cardiomyopathy and a potential role for DPP-4 inhibition in prevention and/or correction of oxidant stress/fibrosis and associated diastolic dysfunction.
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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.