ArticleScientific reports2024
SALL4 mediates SHP2 inhibition in myocardial fibroblasts through the DOT1L/H3K79me2 signaling pathway to promote the progression of myocardial infarction.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- The effects of YAP/TAZ in cardiomyocytes: a scoping review.Molecular biology reports · 2025Article
- USP37-stabilized SALL4 promotes the keloid formation by PI3K/AKT pathway.Scientific reports · 2025Article
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Authors and funding
6 authors.
Funding
Abstract
objectiveTo explore the influence of SALL4 in cardiac fibroblasts on the progression of myocardial infarction.
methodsAnalysis of genes specifically expressed in myocardial infarction by bioinformatics methods; The impact of SALL4 on myocardial infarction was assessed using mouse ultrasound experiments and Masson staining; The effect of SALL4 on the expression levels of collagen-I and collagen-III in myocardial tissue was examined by immunohistochemical staining; The migration ability of cardiac fibroblasts was evaluated using a Transwell assay; The proliferative ability of cardiac fibroblasts was tested using a CCK-8 assay; The relative fluorescence intensity of α-SMA and CTGF in cardiac fibroblasts were checked through immunofluorescence staining experiment; The expression of SALL4, DOT1L, H3K79me2, P53, SHP2, YAP, nucleus-YAP, collagen-I, α-SMA, CTGF, and PAI-1 in myocardial tissues or cardiac fibroblasts was detected using western blot analysis.
resultsSALL4-specific high expression in myocardial infarction; SALL4 intensified the alterations in the heart structure of mice with myocardial infarction and worsened the fibrosis of myocardial infarction; SALL4 also promoted the expression of SALL4, DOT1L, H3K79me2, P53, SHP2, YAP, nucleus-YAP, collagen-I, collagen-III, α-SMA, CTGF, and PAI-1 in myocardial infarction tissues and cardiac fibroblasts; Subsequently, SALL4 could enhance the immunofluorescence intensity of α-SMA and CTGF; Moreover, SALL4 could promote the proliferation and migration of cardiac fibroblasts.
conclusionIn cardiac fibroblasts, SALL4 mediates the DOT1L/H3K79me2 signaling pathway to inhibit SHP2, which then promotes the YAP/TAZ signaling pathway, thereby facilitating the progression of myocardial infarction.
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