ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2025
Dipeptidyl peptidase-4 deficiency prevents chronic stress-induced cardiac remodeling and dysfunction in mice.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Liraglutide Ameliorates Injury-Related Vascular Repair by Activating Autophagy Through Modulation of the PI3K-mTOR Signaling Pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- CD8FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Increased Dipeptidyl Peptidase-4 Promotes Adipose Inflammation and Dysfunction in Mice Under Chronic Stress.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Single-nucleus profiling of the left ventricle of the mouse heart after chronic stress.Scientific data · 2025Article
- Dexmedetomidine Reduces Chronic Stress-Related Thrombosis in a Mouse FeClFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Dipeptidyl peptidase-4 deficiency prevents chronic stress-induced cardiac remodeling and dysfunction in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Exposure to chronic psychosocial stress is a risk factor for metabolic cardiovascular disorders. Dipeptidyl peptidase-4 (DPP-4) plays essential roles in human pathobiology, and we recently showed that DPP-4 levels are increased by chronic stress in murine models. We here investigated the role of DPP-4 in stress-related cardiac injury and dysfunction in mice, focusing on oxidative stress and cardiac apoptosis. Male mice were randomly assigned to non-stress and two-week immobilized-stress groups for biological and morphological studies. On day 14 post-stress, stress had increased blood pressure, heart weight, cardiac myocyte size, and interstitial fibrosis, impaired cardiac diastolic function, and increased plasma levels of DPP-4 and glucose. The stressed mice also had increased levels of monocyte chemoattractant protein-1, inteleukin-6, gp91
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