ArticleScience China. Life sciences2021
Pathological matrix stiffness promotes cardiac fibroblast differentiation through the POU2F1 signaling pathway.
Article in Science China. Life sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 26 citations in OpenAlex.
- POU2F1 promotes hypertensive cardiac fibrosis by regulating mitochondrial homeostasis through PINK1/Parkin‑dependent mitophagy.Molecular medicine reports · 2026Article
- Intercellular chemerin-cmklr1 couples epicardial mechanosensing to fibroblasts in pressure overload.Nature communications · 2026Article
- Upregulated lncRNA XIST drives trophoblast dysfunction through targeting miR-545-5p/POU2F1 axis in recurrent spontaneous abortion.American journal of translational research · 2026Article
- A positive feedback loop between FOSB and miR-133b controls colon cancer cell proliferation.Acta biochimica et biophysica Sinica · 2025Article
- Staphylococcus warneri strain XSB102 exacerbates psoriasis and promotes keratinocyte proliferation in imiquimod-induced psoriasis-like dermatitis mice.Archives of microbiology · 2023Article
- Comparative Analysis of Heart Regeneration: Searching for the Key to Heal the Heart-Part II: Molecular Mechanisms of Cardiac Regeneration.Journal of cardiovascular development and disease · 2023Review
- Exercise training attenuates angiotensin II-induced cardiac fibrosis by reducing POU2F1 expression.Journal of sport and health science · 2023Article
- Galectin-3-centered paracrine network mediates cardiac inflammation and fibrosis upon β-adrenergic insult.Science China. Life sciences · 2023Article
- Network model integrated with multi-omic data predicts MBNL1 signals that drive myofibroblast activation.iScience · 2023Article
- Cardiac ischemia on-a-chip to investigate cellular and molecular response of myocardial tissue under hypoxia.Biomaterials · 2022Article
- Machine learning-based integration develops biomarkers initial the crosstalk between inflammation and immune in acute myocardial infarction patients.Frontiers in cardiovascular medicine · 2022Article
- Article
- Identification of potential micro-messenger RNAs (miRNA-mRNA) interaction network of osteosarcoma.Bioengineered · 2021Article
- Construction of miRNA-mRNA network reveals crucial miRNAs and genes in acute myocardial infarction.Journal of biomedical research · 2021Article
- Cell-cell crosstalk in the heart.Medical review (2021) · 2021Article
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Authors and funding
12 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac fibroblast (CF) differentiation into myofibroblasts is a crucial cause of cardiac fibrosis, which increases in the extracellular matrix (ECM) stiffness. The increased stiffness further promotes CF differentiation and fibrosis. However, the molecular mechanism is still unclear. We used bioinformatics analysis to find new candidates that regulate the genes involved in stiffness-induced CF differentiation, and found that there were binding sites for the POU-domain transcription factor, POU2F1 (also known as Oct-1), in the promoters of 50 differentially expressed genes (DEGs) in CFs on the stiffer substrate. Immunofluorescent staining and Western blotting revealed that pathological stiffness upregulated POU2F1 expression and increased CF differentiation on polyacrylamide hydrogel substrates and in mouse myocardial infarction tissue. A chromatin immunoprecipitation assay showed that POU2F1 bound to the promoters of fibrosis repressors IL1R2, CD69, and TGIF2. The expression of these fibrosis repressors was inhibited on pathological substrate stiffness. Knockdown of POU2F1 upregulated these repressors and attenuated CF differentiation on pathological substrate stiffness (35 kPa). Whereas, overexpression of POU2F1 downregulated these repressors and enhanced CF differentiation. In conclusion, pathological stiffness upregulates the transcription factor POU2F1 to promote CF differentiation by inhibiting fibrosis repressors. Our work elucidated the crosstalk between CF differentiation and the ECM and provided a potential target for cardiac fibrosis treatment.
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