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Association of lipoprotein(a) and LPA gene with calcific aortic valve disease

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Název: Association of lipoprotein(a) and LPA gene with calcific aortic valve disease
Autoři: Xinyi Yu, Zean Fu, Minghuan Yu, Yibo Shi
Zdroj: European Journal of Medical Research, Vol 30, Iss 1, Pp 1-11 (2025)
Informace o vydavateli: BMC, 2025.
Rok vydání: 2025
Sbírka: LCC:Medicine
Témata: Calcific aortic valve disease, Aortic valve calcification, Lipoprotein(a), LPA gene, Medicine
Popis: Abstract Objective To investigate the association between Lp(a) levels and calcific aortic valve disease (CAVD) and the potential molecular mechanism underlying the effect of LPA gene expression on aortic valve calcification (AVC). Methods Case–control and cohort studies on the association between Lp(a) and CAVD were searched in the meta-analysis. Meta-analysis was performed using RevMan and Stata. AVC-related gene microarray data were obtained from the GEO database. The Gene Set Variation Analysis (GSVA) algorithm was used to synthetically score each gene set and analyze differences in pathways in the LPA gene high- and low-expression groups. The expression of endothelial markers, interstitial markers and osteogenic markers after Lp(a) intervention in human aortic valve endothelial cells (AVEC) was detected by Western blot. Results The risk of CAVD was increased 1.44-fold (95% CI 1.25–1.67, P 30 mg/dL and 1.95-fold (95% CI 1.93–1.97, P 50 mg/dL. GSVA results showed that high expression of the LPA gene was associated with TGF-β signaling, oxidative phosphorylation, and reactive oxygen species pathway. Western-blot results showed that after Lp(a) was co-cultured with AVEC for 72 h, the expression of endothelial markers decreased, while the expression of interstitial markers and osteogenic markers increased. Conclusion Elevated Lp(a) concentration is a risk factor for CAVD. High expression of the LPA gene (or high concentration of Lp(a)) may cause EndoMT of AVEC by disrupting pathways, such as TGF-β signaling, resulting in CAVD.
Druh dokumentu: article
Popis souboru: electronic resource
Jazyk: English
ISSN: 2047-783X
Relation: https://doaj.org/toc/2047-783X
DOI: 10.1186/s40001-025-03071-8
Přístupová URL adresa: https://doaj.org/article/5841f86796a64e08a65488a77fbf33ac
Přístupové číslo: edsdoj.5841f86796a64e08a65488a77fbf33ac
Databáze: Directory of Open Access Journals
Popis
Abstrakt:Abstract Objective To investigate the association between Lp(a) levels and calcific aortic valve disease (CAVD) and the potential molecular mechanism underlying the effect of LPA gene expression on aortic valve calcification (AVC). Methods Case–control and cohort studies on the association between Lp(a) and CAVD were searched in the meta-analysis. Meta-analysis was performed using RevMan and Stata. AVC-related gene microarray data were obtained from the GEO database. The Gene Set Variation Analysis (GSVA) algorithm was used to synthetically score each gene set and analyze differences in pathways in the LPA gene high- and low-expression groups. The expression of endothelial markers, interstitial markers and osteogenic markers after Lp(a) intervention in human aortic valve endothelial cells (AVEC) was detected by Western blot. Results The risk of CAVD was increased 1.44-fold (95% CI 1.25–1.67, P 30 mg/dL and 1.95-fold (95% CI 1.93–1.97, P 50 mg/dL. GSVA results showed that high expression of the LPA gene was associated with TGF-β signaling, oxidative phosphorylation, and reactive oxygen species pathway. Western-blot results showed that after Lp(a) was co-cultured with AVEC for 72 h, the expression of endothelial markers decreased, while the expression of interstitial markers and osteogenic markers increased. Conclusion Elevated Lp(a) concentration is a risk factor for CAVD. High expression of the LPA gene (or high concentration of Lp(a)) may cause EndoMT of AVEC by disrupting pathways, such as TGF-β signaling, resulting in CAVD.
ISSN:2047783X
DOI:10.1186/s40001-025-03071-8