ArticleJournal of geriatric cardiology : JGC2026
Integrated analyses of single-cell transcriptome and mendelian randomization reveal the role of lymphatic endothelial CD74 in the progression of atherosclerosis.
Article in Journal of geriatric cardiology : JGC, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Lymphatic dysfunction plays a critical role in the development of atherosclerotic plaques, and targeting lymphatic regulation offers promising strategies for preventing and treating atherosclerosis (AS). This study aims to identify key genes influencing AS in lymphatic endothelial cells (LECs) followed by validation, and to explore potential intervention targets for AS treatment. Methods: Single-cell data from the GEO database and Mendelian randomization was employed to identify genes in LECs that may either exacerbate or protect against AS. AS mouse models were established, followed by the assessment of key gene expression in lymphatic vessels within the plaque adventitia. Results: Human carotid plaque data via the GEO database revealed that LEC-specific genes are closely associated with vasculogenesis, cell migration, and inflammatory responses during AS. Mendelian randomization analysis identified CD74 as a promoter of AS progression. Conclusions: This study has identified the key gene CD74 in LECs that influence the progression of AS. Moreover, during AS, CD74 mediates NLRP3/SYK-dependent LEC pyroptosis, thereby inhibiting lymphangiogenesis and exacerbating the inflammatory response. These findings provide a novel molecular mechanism by which CD74 disrupts lymphatic function and accelerates AS progression, offering potential avenues for intervention in AS.
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