We are analyzing https://link.springer.com/article/10.1186/s12933-018-0704-1.

Title:
The role of dipeptidylpeptidase-4 inhibitors in management of cardiovascular disease in diabetes; focus on linagliptin | Cardiovascular Diabetology
Description:
Multiple population based analyses have demonstrated a high incidence of cardiovascular disease (CVD) and cardiovascular (CV) mortality in subjects with T2DM that reduces life expectancy by as much as 15 years. Importantly, the CV system is particularly sensitive to the metabolic and immune derangements present in obese pre-diabetic and diabetic individuals; consequently, CV dysfunction is often the initial CV derangement to occur and promotes the progression to end organ/tissue damage in T2DM. Specifically, diabetic CVD can manifest as microvascular complications, such as nephropathy, retinopathy, and neuropathy, as well as, macrovascular impairments, including ischemic heart disease, peripheral vascular disease, and cerebrovascular disease. Despite some progress in prevention and treatment of CVD, mainly via blood pressure and dyslipidemia control strategies, the impact of metabolic disease on CV outcomes is still a major challenge and persists in proportion to the epidemics of obesity and diabetes. There is abundant pre-clinical and clinical evidence implicating the DPP-4-incretin axis in CVD. In this regard, linagliptin is a unique DPP-4 inhibitor with both CV and renal safety profiles. Moreover, it exerts beneficial CV effects beyond glycemic control and beyond class effects. Linagliptin is protective for both macrovascular and microvascular complications of diabetes in preclinical models, as well as clinical models. Given the role of endothelial-immune cell interactions as one of the key events in the initiation and progression of CVD, linagliptin modulates these cell–cell interactions by affecting two important pathways involving stimulation of NO signaling and potent inhibition of a key immunoregulatory molecule.
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Keywords {🔍}

pubmed, article, google, scholar, cas, diabetes, linagliptin, dpp, effects, central, inhibitors, type, patients, cardiovascular, vascular, function, disease, dipeptidyl, peptidase, inhibitor, heart, dysfunction, risk, diabetic, clinical, inhibition, tdm, signaling, endothelial, myocardial, tissue, obesity, hypertension, mice, cells, insulin, glp, mechanisms, cardiovasc, study, control, outcomes, therapy, studies, klotho, recent, stiffness, cardiac, receptor, including,

Topics {✒️}

nf-κb nuclear factor-kappa long-term incretin-based therapies dendritic cell/macrophage-expressing dpp4 tissue renin-angiotensin-aldosterone system article download pdf stromal cell-derived factor-1 aldosterone-induced cardiomyocyte growth renin-angiotensin-aldosterone system dipeptidyl peptidase-iv inhibitor end organ/tissue damage tlr2-mediated cerebrovascular hyperreactivity wd-induced aortic stiffness aortic-banded mini-swine central artery stiffness t-cell surface marker at1/at2 receptor expression investigate short-term effects myocardial ischaemia-reperfusion injury glp-1r glp-1 receptor elevated circulating alpha-klotho myocardial ischemia–reperfusion injury angiotensin receptor blocker streptozotocin-induced diabetic mice vitamin d-fgf-23-klotho stroke utilizing middle-aged streptozotocin-induced diabetic rats pre-clinical diastolic dysfunction central nervous system circulating progenitor/stem cells camila manrique-acevedo & vincent c57bl/6j background excess nutrient consumption/obesity population-based cohort study single-pill combination therapy dpp-4 inhibitor-mediated targeting wd-western diet long-term cv safety low-dose sitagliptin dendritic cell/macrophages contributes dipeptidyl-peptidase-4 inhibition therapy de boer ra obesity-induced visceral inflammation macrophage inflammatory protein-1α intensive glucose-lowering regimen preserved ejection fraction org/content/41/supplement_1/s55 age-related aortic stiffening mediate anti-inflammatory effects endothelial-immune cell interactions placebo-controlled clinical trial

Questions {❓}

Dipeptidyl peptidase inhibitors, an emerging drug class for inflammatory disease?
Have dipeptidyl peptidase-4 inhibitors ameliorated the vascular complications of type 2 diabetes in large-scale trials?
Initial combination therapy for type 2 diabetes mellitus: is it ready for prime time?
Is glucose control important for prevention of cardiovascular disease in diabetes?
Mmp-9 inhibitors in the brain: can old bullets shoot new targets?
The gut-renal axis: do incretin-based agents confer renoprotection in diabetes?

Schema {🗺️}

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         description:Multiple population based analyses have demonstrated a high incidence of cardiovascular disease (CVD) and cardiovascular (CV) mortality in subjects with T2DM that reduces life expectancy by as much as 15 years. Importantly, the CV system is particularly sensitive to the metabolic and immune derangements present in obese pre-diabetic and diabetic individuals; consequently, CV dysfunction is often the initial CV derangement to occur and promotes the progression to end organ/tissue damage in T2DM. Specifically, diabetic CVD can manifest as microvascular complications, such as nephropathy, retinopathy, and neuropathy, as well as, macrovascular impairments, including ischemic heart disease, peripheral vascular disease, and cerebrovascular disease. Despite some progress in prevention and treatment of CVD, mainly via blood pressure and dyslipidemia control strategies, the impact of metabolic disease on CV outcomes is still a major challenge and persists in proportion to the epidemics of obesity and diabetes. There is abundant pre-clinical and clinical evidence implicating the DPP-4-incretin axis in CVD. In this regard, linagliptin is a unique DPP-4 inhibitor with both CV and renal safety profiles. Moreover, it exerts beneficial CV effects beyond glycemic control and beyond class effects. Linagliptin is protective for both macrovascular and microvascular complications of diabetes in preclinical models, as well as clinical models. Given the role of endothelial-immune cell interactions as one of the key events in the initiation and progression of CVD, linagliptin modulates these cell–cell interactions by affecting two important pathways involving stimulation of NO signaling and potent inhibition of a key immunoregulatory molecule.
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      headline:The role of dipeptidylpeptidase-4 inhibitors in management of cardiovascular disease in diabetes; focus on linagliptin
      description:Multiple population based analyses have demonstrated a high incidence of cardiovascular disease (CVD) and cardiovascular (CV) mortality in subjects with T2DM that reduces life expectancy by as much as 15 years. Importantly, the CV system is particularly sensitive to the metabolic and immune derangements present in obese pre-diabetic and diabetic individuals; consequently, CV dysfunction is often the initial CV derangement to occur and promotes the progression to end organ/tissue damage in T2DM. Specifically, diabetic CVD can manifest as microvascular complications, such as nephropathy, retinopathy, and neuropathy, as well as, macrovascular impairments, including ischemic heart disease, peripheral vascular disease, and cerebrovascular disease. Despite some progress in prevention and treatment of CVD, mainly via blood pressure and dyslipidemia control strategies, the impact of metabolic disease on CV outcomes is still a major challenge and persists in proportion to the epidemics of obesity and diabetes. There is abundant pre-clinical and clinical evidence implicating the DPP-4-incretin axis in CVD. In this regard, linagliptin is a unique DPP-4 inhibitor with both CV and renal safety profiles. Moreover, it exerts beneficial CV effects beyond glycemic control and beyond class effects. Linagliptin is protective for both macrovascular and microvascular complications of diabetes in preclinical models, as well as clinical models. Given the role of endothelial-immune cell interactions as one of the key events in the initiation and progression of CVD, linagliptin modulates these cell–cell interactions by affecting two important pathways involving stimulation of NO signaling and potent inhibition of a key immunoregulatory molecule.
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