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

Berberine ameliorates atherosclerosis by inhibiting the phenotypic transition of vascular smooth muscle cells via suppression of the JAK2/STAT3 signaling pathway.

European journal of pharmacology - 15 Nov 2025

Zheng Junmeng, Wang Tingting, Zhou Yang, Chen Yushan, Shen Xiangli, Jin Boyuan, Han Xinyi, Hua Chengjun, Xie JinHong

Abstract excerpt

Atherosclerosis (AS) is a widespread cardiovascular disease that significantly impacts human health. This study aimed to investigate the anti-atherosclerotic effects of berberine (BBR) and elucidate its mechanisms through animal and cellular experiments. Apolipoprotein E-deficient (ApoE-/-) mice were fed a high-fat diet for 12 weeks to induce AS. The mice were subjected to the corresponding interventions for 4...

Read the complete abstract on PubMed

Topics

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

Share to Apolipoproteins E
Share to Atherosclerosis

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Janus Kinase 2

Share to Lipoproteins, LDL

Share to Mice, Knockout, ApoE

Share to Muscle, Smooth, Vascular

Share to Myocytes, Smooth Muscle

Share to STAT3 Transcription Factor

Source

Identifiers

PMID: 41075918
DOI: 10.1016/j.ejphar.2025.178234

Genes

STAT3
JAK2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Berberine ameliorates atherosclerosis by inhibiting the phenotypic transition of vascular smooth muscle cells via suppression of the JAK2/STAT3 signaling pathway.PMID 41075918Read ↗

Paeoniflorin suppresses the phenotypic transformation of vascular smooth muscle cells during atherosclerosis by regulating the MAPK/NF-κB pathways and ABCA1 expression.Semantic proximity Read ↗

Berberine Inhibits Abdominal Aortic Aneurysm Formation and Vascular Smooth Muscle Cell Phenotypic Switching by Regulating the Nrf2 Pathway.Semantic proximity Read ↗

Effect of sinomenine on vascular smooth muscle cell dedifferentiation and neointima formation after vascular injury in mice.Semantic proximity Read ↗

Quercetin Attenuates KLF4-Mediated Phenotypic Switch of VSMCs to Macrophage-like Cells in Atherosclerosis: A Critical Role for the JAK2/STAT3 Pathway.Semantic proximity Read ↗

Piperlonguminine attenuates atherosclerosis in mice via phenotype switching inhibition of vascular smooth muscle cells.Semantic proximity Read ↗

The Role of JAK/STAT Signaling Pathway and Its Downstream Influencing Factors in the Treatment of AtherosclerosisSemantic proximity Read ↗

Attenuating Effects of Pyrogallol-Phloroglucinol-6,6-Bieckol on Vascular Smooth Muscle Cell Phenotype Changes to Osteoblastic Cells and Vascular Calcification Induced by High Fat Diet.Semantic proximity Read ↗

Crocin prevents platelet‑derived growth factor BB‑induced vascular smooth muscle cells proliferation and phenotypic switch.Semantic proximity Read ↗

Anti-atherosclerotic plants which modulate the phenotype of vascular smooth muscle cells.Semantic proximity Read ↗

Network Pharmacology-Based Investigation on the Mechanism of Aloin in Ameliorating Atherosclerosis by Regulating Macrophage PolarizationSemantic proximity Read ↗

7-O-methylpunctatin, a Novel Homoisoflavonoid, Inhibits Phenotypic Switch of Human Arteriolar Smooth Muscle Cells.Semantic proximity Read ↗

Xuefu Zhuyu decoction attenuates thoracic aortic dissection by regulating VSMC phenotypic switching and oxidative stress via the JAK2/STAT3/HIF-1α pathway.Semantic proximity Read ↗

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