ArticleActa pharmacologica Sinica2024
Par3L, a polarity protein, promotes M1 macrophage polarization and aggravates atherosclerosis in mice via p65 and ERK activation.
Article in Acta pharmacologica Sinica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- SPP1+ macrophages contribute to silica-induced pulmonary inflammation and fibrosis via the ERK/JNK signaling pathway.American journal of respiratory cell and molecular biology · 2026Article
- A Mesoporous Silica-Based Naringenin Delivery System Promoting Macrophage M2 Polarization in Atherosclerosis.Biomaterials research · 2025Article
- Potential of herbal formulas and bioactive metabolites in treating atherosclerosis: targeted modulation of macrophage polarization.Frontiers in pharmacology · 2025Review
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proinflammatory M1 macrophages are critical for the progression of atherosclerosis. The Par3-like protein (Par3L) is a homolog of the Par3 family involved in cell polarity establishment. Par3L has been shown to maintain the stemness of mammary stem cells and promote the survival of colorectal cancer cells. In this study, we investigated the roles of the polar protein Par3L in M1 macrophage polarization and atherosclerosis. To induce atherosclerosis, Apoe
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