Updated Role of Neuropeptide Y in Nicotine-Induced Endothelial Dysfunction and Atherosclerosis

Yanli, Zheng; Wang, Wan-da; Li, Meimei; Lin, Shu; Lin, Haiyan

doi:10.3389/fcvm.2021.630968

Cited by 15 publications

(6 citation statements)

References 119 publications

(92 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These factors will be harmful to the arteries, and promote the development of atherosclerosis (67,74). Other studies have found that Neuropeptide Y (NPY) is a mediator of vascular lipid metabolism disorder under chronic stress and a risk factor for stress-induced lipid metabolic syndrome and atherosclerosis (75)(76)(77)(78). Understanding how neuropeptide Y and its homologous receptors regulate lipid metabolism may provide new ideas for the study of the mechanism and treatment of atherosclerosis (79,80).…”

Section: Disorder Of Lipid Metabolism In Atherosclerosis Under Chronic Stressmentioning

confidence: 99%

Chronic Stress A Potential Suspect Zero of Atherosclerosis: A Systematic Review

Meng

Zhang

Luo³

et al. 2021

Front. Cardiovasc. Med.

View full text Add to dashboard Cite

Atherosclerosis (AS) is a chronic vascular inflammatory disease, in which the lipid accumulation in the intima of the arteries shows yellow atheromatous appearance, which is the pathological basis of many diseases, such as coronary artery disease, peripheral artery disease and cerebrovascular disease. In recent years, it has become the main cause of death in the global aging society, which seriously endangers human health. As a result, research on AS is increasing. Lesions of atherosclerosis contain macrophages, T cells and other cells of the immune response, together with cholesterol that infiltrates from the blood. Recent studies have shown that chronic stress plays an important role in the occurrence and development of AS. From the etiology of disease, social, environmental and genetic factors jointly determine the occurrence of disease. Atherosclerotic cardio-cerebrovascular disease (ASCVD) is often caused by chronic stress (CS). If it cannot be effectively prevented, there will be biological changes in the body environment successively, and then the morphological changes of the corresponding organs. If the patient has a genetic predisposition and a combination of environmental factors triggers the pathogenesis, then chronic stress can eventually lead to AS. Therefore, this paper discusses the influence of chronic stress on AS in the aspects of inflammation, lipid metabolism, endothelial dysfunction, hemodynamics and blood pressure, plaque stability, autophagy, ferroptosis, and cholesterol efflux.

show abstract

Section: Disorder Of Lipid Metabolism In Atherosclerosis Under Chronic Stressmentioning

confidence: 99%

Chronic Stress A Potential Suspect Zero of Atherosclerosis: A Systematic Review

Meng

Zhang

Luo³

et al. 2021

Front. Cardiovasc. Med.

View full text Add to dashboard Cite

show abstract

“…26 Overexpression of NPY in perivascular regions can promote plaque development and coronary atherosclerotic formation. 27 In this work, we developed a multimodal sensing platform to simultaneously detect Na + , AA, and NPY in sweat, toward a real-time personalized evaluation of the cardiovascular health status (Figure 1). Herein, carbon quantum dots (CQDs) are chosen as electrode substrates to immobilize enzymes and provide reactive sites.…”

Section: ■ Introductionmentioning

confidence: 99%

“…Abnormal Na + levels can lead to unstable intracardiac metabolism resulting in myocardial ischemia and arrhythmias. , AA shows the capability of preventing atherosclerosis formation, stimulating blood coagulation function, and declining lipid levels in the blood. , NPY is an expressive neurotransmitter capable of modulating the immune and metabolic responses associated with an atherosclerosis degree . Overexpression of NPY in perivascular regions can promote plaque development and coronary atherosclerotic formation …”

Section: Introductionmentioning

confidence: 99%

A Portable Sweat Sensor Based on Carbon Quantum Dots for Multiplex Detection of Cardiovascular Health Biomarkers

et al. 2022

View full text Add to dashboard Cite

The future of personalized diagnostics and treatment of cardiovascular diseases lies in the use of portable sensors. Portable sensors can acquire biomarker information in biological fluids such as sweat, an approach that mitigates the shortcomings of conventional hospital-centered healthcare. Low sensitivity, selectivity, and specificity remain bottlenecks for the widespread use of portable sensors. Herein, we demonstrate a portable sensor that simultaneously detects Na+, ascorbic acid, and human neuropeptide Y in sweat, all useful biomarkers to index cardiovascular health. The portable sensor comprises a six-electrode system containing three working electrodes, two reference electrodes, and one counter electrode. The working electrodes were prepared by depositing sensing components on carbon quantum dot (CQD) electrodes. The sensing mechanisms were based on selective ion recognition, enzyme catalytic reaction, and immune response, which guarantees specificity to corresponding targets. The CQDs offer massive reactive sites and effectively reduce the interfacial impedance during the sensing reaction, thereby enhancing the three biomarkers’ detection sensitivity. As evidence of portable sensor capability, we demonstrate herein its effective simultaneous detection of the three biomarkers in a real sweat from healthy volunteers during routine activities including exercise, extra ascorbic acid ingestion, and extra Na+ ingestion. As such, the sensor shows promise for real-time noninvasive personalized medical diagnostics and metabolic wellness management.

show abstract

“…Although the best medical treatment and coronary artery reperfusion therapy improve the survival of patients, coronary heart disease is still one of the main causes of morbidity and mortality worldwide. Acute myocardial infarction (AMI) is characterized by the loss of cardiomyocytes, scarring, ventricular remodelling, and can develop into end-stage heart failure [ 1 ]. Therefore, effective cardiac repair is essential for the recovery of cardiac function after AMI.…”

Section: Introductionmentioning

confidence: 99%

Stem cell-derived exosomes in the treatment of acute myocardial infarction in preclinical animal models: a meta-analysis of randomized controlled trials

et al. 2022

Self Cite

View full text Add to dashboard Cite

Background Exosomes (EXOs) derived from stem cells have become a potential new treatment for acute myocardial infarction (AMI). However, their impact is still not fully understood. Therefore, we performed this meta-analysis to systematically review the efficacy of EXOs on AMI in preclinical animal models. Methods We searched PubMed, EMBASE, and the Web of Science from September 1, 1980 to September 1, 2021, to retrieve the studies reporting the therapeutic effects of EXOs on AMI animal models. Secondary endpoints include the fractional shortening (FS), infarct size (IS), fibrosis area (FA), the TNF-α, IL-6 and IL-10 levels, the apoptosis rate and the number of autophagic vesicles. Two authors independently screened the articles based on inclusion and exclusion criteria. All statistical analyses were conducted using Stata14.0. Results Ten studies satisfied the inclusion criteria. Pooled analyses demonstrated that the levels of LVEF (WMD = 3.67%; 95% CI 2.28–5.07%; P = 0.000), FS (WMD = 3.69%; 95% CI 2.06–5.33%; P = 0.000), IS (WMD = −4.52%, 95% CI − 7.14 to − 1.9%; P = 0.001), and FA (WMD = −7.04%, 95% CI − 8.74 to − 5.34%; P = 0.000), TNF-α (WMD = −3.09, 95% CI − 5.47 to − 0.72; P = 0.011), TL-6 (WMD = −6.34, 95% CI − 11.2 to − 1.49; P < 0.01), TL-10 (WMD = 6.37, 95% CI 1.53–11.21; P = 0.01), the apoptosis rate (WMD = −8.23, 95% CI − 15.29 to − 1.17; P = 0.000), and the number of autophagic vesicles (WMD = −4.52, 95% CI − 7.43 to − 1.62; P = 0.000). Subgroup analysis showed that the EXOs were derived from HMSCs. Subgroup analysis showed that the EXOs derived from HMSCs, and that exosome therapy immediately after myocardial infarction can better improve the LVEF. Conclusions: EXOs therapy has the potential to improve cardiac function, fibrogenesis, and inflammatory response, as well as reducing cell apoptosis and autophagy in preclinical AMI animal models. This can inform future human clinical trials of EXOs.

show abstract

Updated Role of Neuropeptide Y in Nicotine-Induced Endothelial Dysfunction and Atherosclerosis

Cited by 15 publications

References 119 publications

Chronic Stress A Potential Suspect Zero of Atherosclerosis: A Systematic Review

Chronic Stress A Potential Suspect Zero of Atherosclerosis: A Systematic Review

A Portable Sweat Sensor Based on Carbon Quantum Dots for Multiplex Detection of Cardiovascular Health Biomarkers

Stem cell-derived exosomes in the treatment of acute myocardial infarction in preclinical animal models: a meta-analysis of randomized controlled trials

Contact Info

Product

Resources

About