ArticleRegenerative therapy2025
Modified bFGF targeting connective tissue growth factor in the injured microenvironment improved cardiac repair after chronic myocardial ischemia.
Article in Regenerative therapy, 2025. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- THR-123, a novel BMP-7 mimetic that activates Akt phosphorylation and inhibits cardiomyocyte apoptosis and inflammation, protects the heart from myocardial injury in a Rat model.Frontiers in cardiovascular medicine · 2026Article
- Mechanisms, strategies, and clinical application progress of subcutaneous transplantation angiogenesis.Frontiers in bioengineering and biotechnology · 2025Review
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Authors and funding
10 authors.
Funding
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Abstract
Myocardial infarction (MI) was a cardiovascular emergency that led to heart failure, arrhythmia, and sudden death. Basic fibroblast growth factor (bFGF) was revealed to promote angiogenesis and protect cardiomyocytes against ischemic injury. But conventional delivery of bFGF in an uncontrolled manner was inefficient and diffusive, limiting its application in MI therapy. Currently, stimuli-responsive drug delivery is emphasized in tissue regeneration. The present study constructed a CFBP-bFGF recombinant protein, which could specifically target upregulated connective tissue growth factor (CTGF) and release bFGF in ischemic myocardium. In a rat model with MI, intravenous administration of CFBP-bFGF significantly accumulated in ischemic myocardium by targeting with CTGF. The responsive release of CFBP-bFGF effectively enhanced blood vessel regeneration, decreased cardiomyocyte apoptosis, and improved cardiac function recovery. In addition, the molecular mechanism was further explored by RNA sequencing and transcriptome analysis. Besides activating the pathways and genes related to angiogenesis and cardiac protection, CFBP-bFGF also decreased the expression of fibrosis-related pathways and genes, such as TGF-β. These results demonstrated that the CTGF-responsive CFBP-bFGF was effective for targeting release that promoted the functional recovery of MI.
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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 Socratic graph.