Cardiovascular effects of Glucagon-like peptide 1 (GLP-1) receptor agonists DOI Creative Commons

Francisco Saraiva,

Andrei C. Spósito

Cardiovascular Diabetology, Journal Year: 2014, Volume and Issue: 13(1)

Published: Oct. 22, 2014

Patients with type 2 diabetes have a several-fold increased risk of developing cardiovascular disease when compared nondiabetic controls. Myocardial infarction and stroke are responsible for 75% all death in patients diabetes, who present 2-4× incidence from coronary artery disease. considered secondary prevention because their level is similar to that reported without already suffered myocardial infarction. More recently, better factors control, mainly intensive LDL cholesterol targets statins, significant decrease acute events was observed population diabetes. Together other major factors, must be as an important cause Glucagon like peptide-1 receptor agonists represent novel class anti-hyperglycemic agents cardiac-friendly profile, preserve neuronal cells inhibit degeneration, anti-inflammatory effect liver protecting it against steatosis, increase insulin sensitivity, promote weight loss, satiety or anorexia. This review intended rationally compile the multifactorial effects glucagon-like available treatment

Language: Английский

Glucagon-like peptide 1 (GLP-1) DOI Creative Commons
Timo D. Müller, Brian Finan, Stephen R. Bloom

et al.

Molecular Metabolism, Journal Year: 2019, Volume and Issue: 30, P. 72 - 130

Published: Sept. 30, 2019

Background: The glucagon-like peptide-1 (GLP-1) is a multifaceted hormone with broad pharmacological potential.Among the numerous metabolic effects of GLP-1 are glucose-dependent stimulation insulin secretion, decrease gastric emptying, inhibition food intake, increase natriuresis and diuresis, modulation rodent b-cell proliferation.GLP-1 also has cardio-and neuroprotective effects, decreases inflammation apoptosis, implications for learning memory, reward behavior, palatability.Biochemically modified enhanced potency sustained action, receptor agonists successfully in clinical use treatment type-2 diabetes, several GLP-1-based pharmacotherapies evaluation obesity.Scope review: In this review, we provide detailed overview on nature its pharmacology discuss therapeutic various diseases.Major conclusions: Since discovery, emerged as pleiotropic myriad functions that go well beyond classical identification an incretin hormone.The beneficial render interesting candidate development to treat obesity, neurodegenerative disorders

Language: Английский

Citations

1312

Mammalian MAPK Signal Transduction Pathways Activated by Stress and Inflammation: A 10-Year Update DOI

John Kyriakis,

Joseph Avruch

Physiological Reviews, Journal Year: 2012, Volume and Issue: 92(2), P. 689 - 737

Published: April 1, 2012

The mammalian stress-activated families of mitogen-activated protein kinases (MAPKs) were first elucidated in 1994, and by 2001, substantial progress had been made identifying the architecture pathways upstream these as well cataloguing candidate substrates. This information remains largely sound. Nevertheless, an informed understanding physiological pathophysiological roles remained to be accomplished. In past decade, there has explosion new work using RNAi cells, transgenic, knockout conditional technology mice that provided valuable insight into functions MAPK pathways. These findings have important implications our organ development, innate acquired immunity, diseases such atherosclerosis, tumorigenesis, type 2 diabetes. developments bring us within striking distance development validation novel treatment strategies. Herein we summarize molecular components stress-regulated their regulation described thus far. We then review some vivo

Language: Английский

Citations

1273

Mechanisms of physiological and pathological cardiac hypertrophy DOI
Michinari Nakamura, Junichi Sadoshima

Nature Reviews Cardiology, Journal Year: 2018, Volume and Issue: 15(7), P. 387 - 407

Published: April 19, 2018

Language: Английский

Citations

1267

Pathophysiology of cardiac hypertrophy and heart failure: signaling pathways and novel therapeutic targets DOI
Yow Keat Tham, Bianca C. Bernardo, Jenny Y. Y. Ooi

et al.

Archives of Toxicology, Journal Year: 2015, Volume and Issue: 89(9), P. 1401 - 1438

Published: Feb. 23, 2015

Language: Английский

Citations

611

Diabetic cardiomyopathy: Mechanisms and new treatment strategies targeting antioxidant signaling pathways DOI

Karina Huynh,

Bianca C. Bernardo, Julie R. McMullen

et al.

Pharmacology & Therapeutics, Journal Year: 2014, Volume and Issue: 142(3), P. 375 - 415

Published: Jan. 22, 2014

Language: Английский

Citations

513

Cardiovascular Biology of the Incretin System DOI Open Access
John R. Ussher, Daniel J. Drucker

Endocrine Reviews, Journal Year: 2012, Volume and Issue: 33(2), P. 187 - 215

Published: Feb. 8, 2012

Glucagon-like peptide-1 (GLP-1) is an incretin hormone that enhances glucose-stimulated insulin secretion and exerts direct indirect actions on the cardiovascular system. GLP-1 its related hormone, glucose-dependent insulinotropic polypeptide, are rapidly inactivated by enzyme dipeptidyl peptidase 4 (DPP-4), a key determinant of bioactivity. Two classes medications enhance action, receptor (GLP-1R) agonists DPP-4 inhibitors, used for treatment type 2 diabetes mellitus. We review herein biology GLP-1R including effects cardiomyocytes, blood vessels, adipocytes, control pressure, postprandial lipoprotein secretion. Both activation inhibition exert multiple cardioprotective in preclinical models dysfunction, short-term studies human subjects appear to demonstrate modest yet beneficial cardiac function with ischemic heart disease. Incretin-based agents body weight, improve glycemic low risk hypoglycemia, decrease inhibit intestinal chylomicrons, reduce inflammation studies. Nevertheless, there limited information these patients established Hence, more complete understanding benefit ratio incretin-based therapies will require completion long-term outcome currently underway

Language: Английский

Citations

510

Signaling pathways and targeted therapy for myocardial infarction DOI Creative Commons
Qing Zhang, Lu Wang, Shiqi Wang

et al.

Signal Transduction and Targeted Therapy, Journal Year: 2022, Volume and Issue: 7(1)

Published: March 10, 2022

Abstract Although the treatment of myocardial infarction (MI) has improved considerably, it is still a worldwide disease with high morbidity and mortality. Whilst there long way to go for discovering ideal treatments, therapeutic strategies committed cardioprotection cardiac repair following ischemia are emerging. Evidence pathological characteristics in MI illustrates cell signaling pathways that participate survival, proliferation, apoptosis, autophagy cardiomyocytes, endothelial cells, fibroblasts, monocytes, stem cells. These include key players inflammation response, e.g., NLRP3/caspase-1 TLR4/MyD88/NF-κB; crucial mediators oxidative stress instance, Notch, Hippo/YAP, RhoA/ROCK, Nrf2/HO-1, Sonic hedgehog; controller fibrosis such as TGF-β/SMADs Wnt/β-catenin; main regulator angiogenesis, PI3K/Akt, MAPK, JAK/STAT, hedgehog, etc. Since play an important role administering process MI, aiming at targeting these aberrant improving manifestations indispensable promising. Hence, drug therapy, gene protein exosome therapy have been emerging known novel therapies. In this review, we summarize by regulating associated pathways, which contribute inhibiting cardiomyocytes death, attenuating inflammation, enhancing so re-functionalize damaged hearts.

Language: Английский

Citations

479

Signaling effectors underlying pathologic growth and remodeling of the heart DOI Open Access
Jop H. van Berlo,

Marjorie Maillet,

Jeffery D. Molkentin

et al.

Journal of Clinical Investigation, Journal Year: 2013, Volume and Issue: 123(1), P. 37 - 45

Published: Jan. 2, 2013

Cardiovascular disease is the number one cause of mortality in Western world. The heart responds to many cardiopathological conditions with hypertrophic growth by enlarging individual myocytes augment cardiac pump function and decrease ventricular wall tension. Initially, such often compensatory, but as time progresses these changes become maladaptive. Cardiac hypertrophy strongest predictor for development failure, arrhythmia, sudden death. Here we discuss therapeutic avenues emerging from molecular genetic studies cardiovascular animal models. majority are based on intracellular signaling pathways considered central pathologic remodeling hypertrophy, which then leads failure. We focus our discussion selected targets that have more recently emerged a tangible translational potential given available pharmacologic agents could be readily evaluated human clinical trials.

Language: Английский

Citations

407

Recent progress regarding kaempferol for the treatment of various diseases (Review) DOI Open Access
Jie Ren, Yifei Lü,

Yanhong Qian

et al.

Experimental and Therapeutic Medicine, Journal Year: 2019, Volume and Issue: unknown

Published: Aug. 13, 2019

Kaempferol, also known as kaempferol‑3 or kaempferide, is a flavonoid compound that naturally occurs in tea, well numerous common vegetables and fruits, including beans, broccoli, cabbage, gooseberries, grapes, kale, strawberries, tomatoes, citrus brussel sprouts, apples grapefruit. The present review mainly summarizes the application of kaempferol treating diseases underlying mechanisms are currently being studied. Due to its anti‑inflammatory properties, it may be used treat acute chronic inflammation‑induced diseases, intervertebral disc degeneration colitis, post‑menopausal bone loss lung injury. In addition, has beneficial effects against cancer, liver injury, obesity diabetes, inhibits vascular endothelial inflammation, protects cranial nerve heart function, for fibroproliferative disorders, hypertrophic scar

Language: Английский

Citations

223

Mechanisms contributing to cardiac remodelling DOI
Qingqing Wu, Yang Xiao, Yuan Yuan

et al.

Clinical Science, Journal Year: 2017, Volume and Issue: 131(18), P. 2319 - 2345

Published: Aug. 25, 2017

Cardiac remodelling is classified as physiological (in response to growth, exercise and pregnancy) or pathological inflammation, ischaemia, ischaemia/reperfusion (I/R) injury, biomechanical stress, excess neurohormonal activation afterload). Physiological of the heart characterized by a fine-tuned orchestrated process beneficial adaptations. Pathological cardiac structural functional changes in left ventricle (LV) internal external cardiovascular damage influence pathogenic risk factors, precursor clinical failure (HF). associated with fibrosis, inflammation cellular dysfunction (e.g. abnormal cardiomyocyte/non-cardiomyocyte interactions, oxidative endoplasmic reticulum (ER) autophagy alterations, impairment metabolism signalling pathways), leading HF. This review describes key molecular responses involved remodelling.

Language: Английский

Citations

184