ArticleDrug design, development and therapy2025
Geniposide Stabilized Atherosclerosis Plaque by Induced M2 Polarization via PPARγ Signaling Pathway.
Article in Drug design, development and therapy, 2025. 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.
- Qinggan Jianpi formula attenuates atherosclerosis by suppressing macrophage lactate transport to activate repair genes via H3K18 lactylation.Chinese medicine · 2026Article
- GFPT2 promotes macrophage dysfunction in atherosclerosis via ACADL glycosylation-dependent suppression of ACADL and Arg1.Cellular and molecular life sciences : CMLS · 2026Article
- Baicalein links macrophage M2 polarization with reduced synovial inflammation to alleviate gouty arthritis.Frontiers in immunology · 2026Article
- Geniposide Stabilized Atherosclerosis Plaque by Induced M2 Polarization via PPARγ Signaling Pathway [Letter].Drug design, development and therapy · 2025Article
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Authors and funding
7 authors.
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Abstract
Objective: The instability of atherosclerotic (AS) plaque constitutes a critical trigger for acute intravascular thrombosis and cardiovascular disease. Prior studies have found that Methods: In vitro, RAW264.7 was used to investigate the effects of Gen on polarization phenotype, anti-inflammatory activity, and its correlation with PPARγ. In vivo, ApoE Results: In vitro, Gen upregulated the expressions of M2 macrophage markers (CD163, IL-10, Arg-1). Moreover, Gen increased the expressions of PPARγ target genes (CD36, ABCG1) and activated PPARγ activity, which could be inhibited by PPARγ antagonist GW9662. In vivo, the intervention of Gen on AS model of ApoE Conclusion: Gen regulates macrophage polarization to M2 phenotype and plays a role in inhibiting inflammation and stabilizing plaque by mediating PPARγ activation, which suggests that Gen may be a promising agent for AS.
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