Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Nesfatin-1 functions as a switch for phenotype transformation and proliferation of VSMCs in hypertensive vascular remodeling.

Biochimica et biophysica acta. Molecular basis of disease - 1 Jun 2018

Lu Qing-Bo, Wang Hui-Ping, Tang Zi-Han, Cheng Han, Du Qiong, Wang Yuan-Ben, Feng Wu-Bing, Li Ke-Xue, Cai Wei-Wei, Qiu Li-Ying, Sun Hai-Jian

Abstract excerpt

The phenotypic transformation from differentiated to dedifferentiated vascular smooth muscle cells (VSMCs) plays a crucial role in VSMC proliferation and vascular remodeling in many cardiovascular diseases including hypertension. Nesfatin-1, a multifunctional adipocytokine, is critically involved in the regulation of blood pressure. However, it is still largely unexplored whether nesfatin-1 is a potential...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Aorta
Share to Gene Knockdown Techniques

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Muscle, Smooth, Vascular

Share to Myocytes, Smooth Muscle

Share to Primary Cell Culture

Share to Rats, Inbred SHR

Share to Rats, Inbred WKY

Share to Vascular Remodeling

Source

Identifiers

PMID: 29627363
DOI: 10.1016/j.bbadis.2018.04.002

Genes

JAK2
STAT3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Nesfatin-1 functions as a switch for phenotype transformation and proliferation of VSMCs in hypertensive vascular remodeling.PMID 29627363Read ↗

Nesfatin-1 regulates the phenotype transition of cavernous smooth muscle cells by activating PI3K/AKT/mTOR signaling pathway to improve diabetic erectile dysfunction.Semantic proximity Read ↗

Elucidating VSMC phenotypic transition mechanisms to bridge insights into cardiovascular disease implicationsSemantic proximity Read ↗

An overview of potential molecular mechanisms involved in VSMC phenotypic modulation.Semantic proximity Read ↗

Signaling pathways regulating vascular smooth muscle cell differentiation.Semantic proximity Read ↗

Six Shades of Vascular Smooth Muscle Cells Illuminated by KLF4 (Krüppel-Like Factor 4).Semantic proximity Read ↗

Role of Krüppel-like factor 4 in phenotypic switching and proliferation of vascular smooth muscle cells.Semantic proximity Read ↗

Vascular Smooth Muscle Cells Phenotypic Switching in Cardiovascular Diseases.Semantic proximity Read ↗

Role of RhoA and Rho-associated kinase in phenotypic switching of vascular smooth muscle cells: Implications for vascular function.Semantic proximity Read ↗

An update on the phenotypic switching of vascular smooth muscle cells in the pathogenesis of atherosclerosis.Semantic proximity Read ↗

Phenotypic switching of vascular smooth muscle cells in atherosclerosis, hypertension, and aortic dissection.Semantic proximity Read ↗

Deficiency of protein inhibitor of activated STAT3 exacerbates atherosclerosis by modulating VSMC phenotypic switching.Semantic proximity Read ↗

Vascular smooth muscle remodeling in health and disease.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.