The Role of Macrophages in Atherosclerosis: Participants and Therapists
Cardiovascular Drugs and Therapy, ISSN: 1573-7241, Vol: 39, Issue: 2, Page: 459-472
2025
- 1Citations
- 5Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Review Description
Currently, atherosclerosis, characterized by the dysfunction of lipid metabolism and chronic inflammation in the intimal space of the vessel, is considered to be a metabolic disease. As the most abundant innate immune cells in the body, macrophages play a key role in the onset, progression, or regression of atherosclerosis. For example, macrophages exhibit several polarization states in response to microenvironmental stimuli; an increasing proportion of macrophages, polarized toward M2, can suppress inflammation, scavenge cell debris and apoptotic cells, and contribute to tissue repair and fibrosis. Additionally, specific exosomes, generated by macrophages containing certain miRNAs and effective efferocytosis of macrophages, are crucial for atherosclerosis. Therefore, macrophages have emerged as a novel potential target for anti-atherosclerosis therapy. This article reviews the role of macrophages in atherosclerosis from different aspects: origin, phenotype, exosomes, and efferocytosis, and discusses new approaches for the treatment of atherosclerosis.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85174604178&origin=inward; http://dx.doi.org/10.1007/s10557-023-07513-5; http://www.ncbi.nlm.nih.gov/pubmed/37864633; https://link.springer.com/10.1007/s10557-023-07513-5; https://dx.doi.org/10.1007/s10557-023-07513-5; https://link.springer.com/article/10.1007/s10557-023-07513-5
Springer Science and Business Media LLC
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