ArticleJournal of translational medicine2014
Inhibition of dipeptidyl peptidase-IV enzyme activity protects against myocardial ischemia-reperfusion injury in rats.
Article in Journal of translational medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 35 citations in OpenAlex.
- High-Density Lipoprotein Treatment Effectively Protected the Endothelial Cells, Mitochondria and Myocardium Against Oxidized Low-Density Lipoprotein Damage.Acta Cardiologica Sinica · 2026Article
- Review
- 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
- Quercetin in Shengxian Decoction exhibits anti-ferroptosis protective roles in a myocardial infarction modelFrontiers in pharmacology · 2025Article
- Omarigliptin inhibits brain cell ferroptosis after intracerebral hemorrhage.Scientific reports · 2023Article
- Yin and Yang of NADPH Oxidases in Myocardial Ischemia-Reperfusion.Antioxidants (Basel, Switzerland) · 2022Review
- Detrimental Effect of Sitagliptin Induced Autophagy on Multiterritory Perforator Flap Survival.Frontiers in pharmacology · 2020Article
- The combination of G9a histone methyltransferase inhibitors with erythropoietin protects heart against damage from acute myocardial infarction.American journal of translational research · 2020Article
- Dipeptidyl Peptidase-4 deficiency effectively protects the brain and neurological function in rodent after acute Hemorrhagic Stroke.International journal of biological sciences · 2020Article
- Early administration of cold water and adipose derived mesenchymal stem cell derived exosome effectively protects the heart from ischemia-reperfusion injury.American journal of translational research · 2019Article
- Combined Therapy with SS31 and Mitochondria Mitigates Myocardial Ischemia-Reperfusion Injury in Rats.International journal of molecular sciences · 2018Article
- Reduced post-operative DPP4 activity associated with worse patient outcome after cardiac surgery.Scientific reports · 2018Observational
- The protective effects of ischemic preconditioning on rats with renal ischemia-reperfusion injury and the effects on the expression of Bcl-2 and Bax.Experimental and therapeutic medicine · 2017Article
- Regulation of Dipeptidyl Peptidase IV in the Post-stroke Rat Brain and In Vitro Ischemia: Implications for Chemokine-Mediated Neural Progenitor Cell Migration and Angiogenesis.Molecular neurobiology · 2017Article
- Administration of antioxidant peptide SS-31 attenuates transverse aortic constriction-induced pulmonary arterial hypertension in mice.Acta pharmacologica Sinica · 2016Article
- Exendin-4 therapy still offered an additional benefit on reducing transverse aortic constriction-induced cardiac hypertrophy-caused myocardial damage in DPP-4 deficient rats.American journal of translational research · 2016Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWe investigated whether attenuating dipeptidyl peptidase-IV (DPP4) enzyme activity protected rat heart from ischemia-reperfusion (IR) injury (40-min left anterior descending coronary artery ligation followed by 72 h reperfusion). METHODS AND
resultsAdult male Fischer 344 rats (n = 24) were equally divided into sham-control (WT-SC), WT-IR, and WT-IR-Sita (oral sitagliptin 400 mg/kg/day for 3 days) groups, whereas adult male DPP4-deficiency (DPP4(D)) rats (n = 16) were equally divided into DPP4(D)-SC and DPP4(D)-IR groups. Animals were sacrificed at 72 h after reperfusion with collection of heart specimens. Infarct area (H&E), collagen deposition (Sirius-red stain), fibrotic area (Masson's trichrome), and fluorescent-ROS intensity (H2DCFDA-labeling myocardium) of left ventricle were significantly higher in WT-IR than those in other groups, significantly higher in WT-IR-Sita and DPP4(D)-IR groups than in WT-SC and DPP4(D)-SC groups (all p < 0.001), but there was no difference between the latter two groups. Protein expressions of oxidative stress (oxidized protein), reactive oxygen species (NOX-1, NOX-2), inflammation (TNF-α, NF-κB, MMP-9, VCAM-1), apoptosis (mitochondrial Bax, cleaved caspase-3 and PARP), myocardial damage markers (cytosolic cytochrome-C, γ-H2AX), and number of inflammatory cells (CD14+, CD68+, CD40+ cells) showed a pattern identical to that of histological changes among all groups (all p < 0.005), whereas markers of anti-apoptosis (Bcl-2) and mitochondrial integrity (mitochondrial cytochrome-C) as well as left ventricular ejection fraction showed an opposite pattern (all p < 0.001). Protein expressions of anti-oxidants (HO-1, NQO-1), angiogenesis factors (SDF-1α, CXCR4), and glycogen-like-peptide-1-receptor were significantly higher inWT-IR-Sita and DPP4(D)-IR than those in other groups (all p <0.001).
conclusionAbrogation of DPP4 activity protects against myocardial IR injury and preserved heart function.
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