ArticleCell death & disease2021
CREG ameliorates the phenotypic switching of cardiac fibroblasts after myocardial infarction via modulation of CDC42.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 25 citations in OpenAlex.
- Single-cell and spatial transcriptomic analyses reveal the dynamic transcript profiles of myocardial lymphangiogenesis post-myocardial infarction.Chinese medical journal · 2026Article
- Trem1 exacerbates myocardial infarction-induced heart failure by inactivating the Rap1 pathway.Journal of cardiothoracic surgery · 2026Article
- Autophagy in High-Fat Diet and Streptozotocin-Induced Metabolic Cardiomyopathy: Mechanisms and Therapeutic Implications.International journal of molecular sciences · 2025Review
- CREG1 restricts ALV-J replication via the mitochondrial dysfunction-driven activation of innate immunity and apoptosis.Frontiers in immunology · 2025Article
- CDC42: unlocking a novel therapeutic target for primary sclerosing cholangitis through Mendelian randomization.American journal of translational research · 2025Article
- CREG1 attenuates doxorubicin-induced cardiotoxicity by inhibiting the ferroptosis of cardiomyocytes.Redox biology · 2024Article
- A Natural Small Molecule Mitigates Kidney Fibrosis by Targeting Cdc42-mediated GSK-3β/β-catenin Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The CREG1-FBXO27-LAMP2 axis alleviates diabetic cardiomyopathy by promoting autophagy in cardiomyocytes.Experimental & molecular medicine · 2023Article
- Dock10 Regulates Cardiac Function under Neurohormonal Stress.International journal of molecular sciences · 2022Article
- Article
- Upregulation of SPI1 during myocardial infarction aggravates cardiac tissue injury and disease progression through activation of the TLR4/NFκB axis.American journal of translational research · 2022Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Phenotype switching of cardiac fibroblasts into myofibroblasts plays important role in cardiac fibrosis following myocardial infarction (MI). Cellular repressor of E1A-stimulated genes (CREG) protects against vascular and cardiac remodeling induced by angiotensin-II. However, the effects and mechanisms of CREG on phenotype switching of cardiac fibroblasts after MI are unknown. This study aimed to investigate the role of CREG on the phenotype switching of cardiac fibroblasts following MI and its mechanism. Our findings demonstrated that, compared with littermate control mice, cardiac function was deteriorated in CREG
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.