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These data indicate that DPP-4 is modulated in a tissue specific manner and is dependent on physiological conditions such as hyperglycaemia and insulin resistance, suggesting a significant role in disorders such as diabetes.
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DPP4 activity when compared to healthy controls. Analysis of Dpp4-Liv-Tg mice revealed elevated systemic DPP4 activity and diminished active GLP-1 levels.
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hepatocyte DPP4 promotes visceral adipose tissue inflammation and insulin resistance in obesity, and targeting this pathway may have metabolic benefits that are distinct from those observed with oral DPP4 inhibitors
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DPP-4 inhibition with linagliptin slowed the progression of premature aging in klotho-/- mice. Provide a novel insight into the potential role of DPP-4 in the mechanism of premature aging.
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Chronic stress accelerates DPP4-mediated GLP-1 degradation and alters plasma adiponectin, accelerating vascular senescence and impairing ischemia-induced neovascularization.
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p53 limits ferroptosis of colorectal cancer cells by blocking DPP4 activity.
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DPP4 can regulate chronic stress-induced hematopoietic stemc cell activation and inflammatory cell production via an Adrbeta3/CXCL12-dependent mechanism that is mediated by the GLP-1/GLP-1R axis.
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DPPIV-knockout mice showed attenuation of scratching in psoriatic pruritus disease model.
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Actions of several substrate chemokines might be potentiated by downregulation of DPP-4, synergistically with upregulation of chemokines and their receptors in adipose tissues of obese mice.
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Inhibition of DPP-4 activity by linagliptin reverses Western diet-induced diastolic dysfunction, possibly by targeting TRAF3IP2 expression and its downstream inflammatory signaling.
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DPP4 is pro-fibrotic in Carbon tetrachloride-induced liver fibrosis.
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systemic DPP4 inhibition restores the impaired mononuclear cell homing in Eng+/- animals post-myocardial infarction, and enhances cardiac repair, which might be explained by restoring the balance between the inflammatory and regenerative macrophages present in the heart
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SGLT-2 inhibition with dapagliflozin reduces the activation of the Nlrp3/ASC inflammasome and attenuates the development of diabetic cardiomyopathy in mice with type 2 diabetes. Effects are augmentated of the by DPP4 inhibitor Saxagliptin.
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DPP-4 inhibitor teneligliptin inhibited atherogenesis in ApoE knockout mice, at least partially, through attenuation of the inflammatory phenotype of perivascular adipose tissue.
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Increased plasma DPP-4 activity may correlate with aneurysmal development. CD26 on monocytes plays a critical role in cell differentiation, possibly mediated by extracellular signal-regulated protein kinase 1/2-p21 axis signaling pathways and cytoskeletal proteins reassembly.
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High DPP4 expression is associated with cardiac ischemia and systolic dysfunction.
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DPP4:CD9:TTSP as the protein complexes are necessary for early efficient MERS-coronavirus entry.
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these findings identify distinct roles for DPP4 in the endothelial cell versus the bone marrow compartment for selective incretin degradation and DPP4 inhibition-mediated glucoregulation.
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The trimeric form receptor-binding domain of MERS-CoV spike protein bound strongly to the receptor of MERS-CoV, dipeptidyl peptidase 4 (DPP4), and elicited robust RBD-specific neutralizing antibodies in mice.
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the data show that glucose-induced expression of Dpp4 in the liver is facilitated by demethylation of the Dpp4 gene early in life. This might contribute to early deteriorations in hepatic function, which in turn result in metabolic disease such as hepatosteatosis later in life.