Li Yang

ORCID: 0000-0003-0234-925X
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About
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Research Areas
  • Signaling Pathways in Disease
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Apelin-related biomedical research
  • Neuropeptides and Animal Physiology
  • Nuclear Receptors and Signaling
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Cardiovascular, Neuropeptides, and Oxidative Stress Research
  • Nitric Oxide and Endothelin Effects
  • Cardiac Fibrosis and Remodeling
  • Protein purification and stability
  • Peptidase Inhibition and Analysis
  • Cell Adhesion Molecules Research
  • Hemoglobin structure and function
  • Caveolin-1 and cellular processes
  • Ultrasound and Hyperthermia Applications

University of South China
2011-2020

The aim of this study was to investigate the role apelin in cell proliferation and autophagy lung adenocarcinoma. over-expression APJ adenocarcinoma detected by immunohistochemistry, while plasma level cancer patients measured enzyme-linked immunosorbent assay. Our findings revealed that apelin-13 significantly increased phosphorylation ERK1/2, expression cyclin D1, microtubule-associated protein 1 light chain 3A/B (LC3A/B), beclin1, confirmed promoted A549 induced via ERK1/2 signaling....

10.1093/abbs/gmt140 article EN Acta Biochimica et Biophysica Sinica 2013-12-30

Abstract Rutaecarpine attenuates hypertensive cardiac hypertrophy in the rats with abdominal artery constriction (AAC); however, its mechanism of action remains largely unknown. Our previous study indicated that NADPH oxidase 4 (Nox4) promotes angiotensin II (Ang II)‐induced through pathway between reactive oxygen species (ROS) and a disintegrin metalloproteinase‐17 (ADAM17) primary cardiomyocytes. This research aimed to determine whether Nox4‐ROS‐ADAM17 is involved protective rutaecarpine...

10.1111/jcmm.14308 article EN cc-by Journal of Cellular and Molecular Medicine 2019-04-05

NADPH oxidases (Noxs) 1/4 dual inhibitor GKT137831 prevents hypertensive cardiac remodelling in angiotensin II-infused transgenic mice with cardiomyocyte-specific human Nox4 (c-hNo x 4 Tg); however, further research is still required to determine the beneficial role of other types models because this model insufficient mimic complicated pathological mechanisms hypertension. A disintegrin and metalloprotease 17 (ADAM17) promotes shedding tumour necrosis factor α (TNF-α), TNF-α receptor,...

10.1016/j.biopha.2018.11.077 article EN Biomedicine & Pharmacotherapy 2018-11-26

Calcitonin gene-related peptide (CGRP) has a potent protective action on the cardiovascular system; however, little is known about role of CGRP in angiotensin II- (Ang II-) induced inflammation vascular smooth muscle cells (VSMCs). This study aimed at determining anti-inflammatory effect Ang II-treated VSMCs and whether disintegrin metalloproteinase 17 (ADAM17) modulates this action. Small interference RNA (siRNA) inhibitors CGRP, epidermal growth factor receptor (EGFR), extracellular...

10.1155/2018/2109352 article EN cc-by Mediators of Inflammation 2018-06-12

Oxidative stress, inflammation, and hypertension constitute a self-perpetuating vicious circle to exacerbate subsequent hypertensive cardiac hypertrophy. NADPH oxidase (Nox) 1/4 inhibitor GKT137831 alleviates hypertrophy in models of secondary hypertension; however, it remains unclear about its effect on essential hypertension. This study is aimed at determining the beneficial role spontaneously rats (SHRs) mechanisms action. Treating with prevented SHRs. Likewise, decreasing production...

10.1155/2020/1078365 article EN cc-by Mediators of Inflammation 2020-08-04

Previous study suggested that the receptor component protein (RCP), one of components calcitonin gene‐related peptide (CGRP) receptor, plays a multiple role in cellular signal transduction. The was designed to investigate whether or not RCP involved regulation caveolin‐1/extracellular signal‐regulated kinases‐1 and ‐2 (ERK1/2) pathway vascular smooth muscle cells (VSMCs) proliferation induced by static pressure. Mouse‐derived VSMCs line A10 (A10 VSMCs) served as project this experiment....

10.1002/jcp.26582 article EN Journal of Cellular Physiology 2018-05-09
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