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Peptidase neurolysin functions to preserve the brain after ischemic stroke in male mice.

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Previous studies documented upregulation of peptidase neurolysin (Nln) after brain ischemia, however the significance of Nln function in the post-stroke brain remained unknown. The aim of this study was to assess the functional role of Nln in the brain after ischemic stroke. Administration of a

The role of peptidase neurolysin in neuroprotection and neural repair after stroke

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Current experimental stroke research has evolved to focus on detailed understanding of the brain's self-protective and restorative mechanisms, and harness this knowledge for development of new therapies. In this context, the role of peptidases and neuropeptides is of growing interest. In this

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.

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Cerebral ischemia evokes abnormal release of proteases in the brain microenvironment that spatiotemporally impact angio-neurogenesis. Dipeptidyl peptidase IV (DPPIV), a cell surface and secreted protease, has been implicated in extracellular matrix remodeling by regulating cell adhesion, migration,

Acute Ischemic Stroke Severity, Progression, and Outcome Relate to Changes in Dipeptidyl Peptidase IV and Fibroblast Activation Protein Activity.

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Dipeptidyl peptidase IV (DPPIV) inhibition may be a promising therapeutic strategy for acute stroke treatment, given its potential to prolong the biological half-life of neuroprotective substrates. A related protease, fibroblast activation protein (FAP), was recently shown to inactivate the same

Dipeptidyl Peptidase-4 Inhibitors for the Potential Treatment of Brain Disorders; A Mini-Review With Special Focus on Linagliptin and Stroke.

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Cerebral stroke is a leading cause of death and persistent disability of elderly in the world. Although stroke prevention by targeting several risk factors such as diabetes and hypertension has decreased the stroke incidence, the total number of strokes is increasing due to the population aging and

Prior treatment with dipeptidyl peptidase 4 inhibitors is associated with better functional outcome and lower in-hospital mortality in patients with type 2 diabetes mellitus admitted with acute ischaemic stroke.

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It is unclear whether prior antidiabetic treatment affects stroke severity and outcome. To evaluate this association, we prospectively studied all patients who were admitted in our Department with acute ischaemic stroke (n = 378, mean age = 78.8 ± 6.5 years). The severity of stroke was assessed at

Dipeptidyl peptidase-4 inhibitors and protection against stroke: A systematic review and meta-analysis.

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BACKGROUND Type 2 diabetes mellitus (T2DM) is associated with an increased risk of stroke and an unfavourable outcome following stroke. Apart from pioglitazone, glucose-lowering modalities have not been shown to protect against stroke. Nevertheless, there is evidence from experimental studies of

Stroke: development, prevention and treatment with peptidase inhibitors.

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Stroke is the leading cause of long-term disability in the United States and affects more people than any other neurologic disorder. Hypertension is a major risk factor associated with stroke. Several anti-hypertensive agents have been used to treat chronic hypertension to reduce the morbidity and

Peptidase neurolysin: Its function related to the brain renin-angiotensin system and pathophysiology of stroke. Letter to the Editor.

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Differential cardiovascular outcomes after dipeptidyl peptidase-4 inhibitor, sulfonylurea, and pioglitazone therapy, all in combination with metformin, for type 2 diabetes: a population-based cohort study.

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OBJECTIVE Data on the comparative effectiveness of oral antidiabetics on cardiovascular outcomes in a clinical practice setting are limited. This study sought to determine whether a differential risk of cardiovascular disease (CVD) exists for the combination of a dipeptidyl peptidase-4 (DPP-4)

Sitagliptin After Ischemic Stroke in Type 2 Diabetic Patients: A Nationwide Cohort Study.

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The cerebrovascular safety and efficacy of sitagliptin, a dipeptidyl peptidase-4 inhibitor, in patients with type 2 diabetes mellitus (T2DM) with ischemic stroke remains uncertain. The aim of this study was to assess the efficacy and safety of sitagliptin in patients with T2DM with recent ischemic

Dipeptidyl peptidase-4 inhibitors and cardiovascular risks in patients with pre-existing heart failure.

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Although recent clinical trials raised concerns about the risk for heart failure (HF) in dipeptidyl peptidase-4 (DPP-4) inhibitor use, data on the cardiovascular risks in the patients with pre-existing HF are still lacking. We used Taiwan's National Health Insurance Research Database to identify 196

Comparative risk for cardiovascular diseases of dipeptidyl peptidase-4 inhibitors vs. sulfonylureas in combination with metformin: Results of a two-phase study.

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The aim was to assess whether the use of additional data from the Disease Management Program (DMP) diabetes mellitus type 2 to minimize the potential for residual confounding will alter the estimated risk of either myocardial infarction, ischemic stroke or heart failure in patients with type 2

Inhibition of circulating dipeptidyl-peptidase 3 restores cardiac function in a sepsis-induced model in rats: A proof of concept study

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Sepsis is a global economic and health burden. Dipeptidyl peptidase 3 (DPP3) is elevated in the plasma of septic patients. The highest levels of circulating DPP3 (cDPP3) are found in non-survivor septic shock patients. The aim of this study was to evaluate the benefits of inhibiting cDPP3 by a

Dipeptidyl peptidase-4 inhibitors do not increase the risk of cardiovascular events in type 2 diabetes: a cohort study.

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OBJECTIVE Two recent randomized controlled trials of type 2 diabetes mellitus (T2DM) patients with history of, or at high risk of, cardiovascular disease (CVD) showed no risk of ischemic cardiovascular events associated with dipeptidyl peptidase-4 inhibitors (DPP4i), but an increased risk of heart

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