ArticlePhysiological reports2025
Elimination of hepatocyte-derived DPP4 downregulates cardiac immune- and collagen-related genes but does not alter cardiac function in aged male mice.
Article in Physiological reports, 2025. 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.
- Extracellular Vesicles Modulation by an Adiponectin Receptor Agonist Provides Cardioprotection for Myocardial Ischemic Injury.Advanced healthcare materials · 2026Article
- 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
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9 authors.
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Abstract
The association between metabolic dysfunction-associated steatotic liver disease (MASLD) and cardiovascular disease is well characterized; however, the underlying mechanism is incompletely understood. Interestingly, hepatocyte-specific silencing of dipeptidyl peptidase 4 (DPP4) prevents liver fibrosis and adipose tissue inflammation; however, how this affects the heart remains to be investigated. This study evaluates how diastolic function and molecular signatures of heart failure, like inflammation and fibrosis, are affected in male Dpp4+/+, Dpp4-/-, and Dpp4flox/flox mice injected with a TBG-CRE to selectively eliminate DPP4 from hepatocytes (Dpp4hep-/-) and respective controls (Dpp4GFP), aged and fed an HFHC diet for 24 weeks. Mice underwent pulsed-wave and tissue Doppler echocardiography. Further, speckle-tracking strain analysis was performed to detect diastolic dysfunction. Differential mRNA analysis using the NanoString platform and qRT-PCR were conducted using ventricular tissue to assess immunological pathway expression, as well as hypertrophy, modeling-related, senescence, and metabolism gene expression. Immunological pathway analysis of ventricular tissue revealed downregulation of 12 immune-related pathways in Dpp4hep-/- mice, including apoptosis and chemokine and cytokine signaling; however, this was not observed in Dpp4-/- mice. Further, fibrosis and ECM modeling-related genes, Col1a1, Col3a1, Ctgf, and Myh7, were significantly upregulated in Dpp4-/- mice but unchanged in Dpp4hep-/- mice, compared to controls. Interestingly, cardiac hypertrophy and systolic and diastolic function evaluated with echocardiography were unchanged. Immune-related pathways are downregulated in Dpp4hep-/- mice, while fibrosis genes are significantly upregulated in Dpp4-/- mice, compared to respective controls. Despite these molecular changes, cardiac hypertrophy and systolic and diastolic function were unchanged with systemic and organ-specific loss of Dpp4.
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