ArticleJournal of cardiovascular translational research2025
Mydgf Enhances Cardiac Angiogenesis by Upregulating FGF1.
Article in Journal of cardiovascular translational research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Human Myeloid-Derived Growth Factor Induces a Pro-Angiogenic Response and Functional Recovery in a Mouse Model of Peripheral Artery Disease.International journal of molecular sciences · 2026Article
- Deep Proteomic Analysis With Machine Learning Identifies Aqueous Humor Biomarkers of ADAMTSL4-associated Congenital Ectopia Lentis.Investigative ophthalmology & visual science · 2026Article
- MYDGF promotes pathological and physiological retinal angiogenesis via the Gαi1/3-Gab1-Akt-mTOR signaling.Nature communications · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Following myocardial infarction (MI), endothelial cell proliferation drives neovascularization to support cardiac regeneration. While myeloid-derived growth factor (Mydgf) is known to promote cardiac repair post-injury, yet its mechanism in angiogenesis remained unclear. In this study, we found that myeloid-derived growth factor knockout (Mydgf-KO) reduced endothelial cell proliferation during early postnatal cardiac angiogenesis and impaired neovascularization post-MI, leading to exacerbated cardiac dysfunction. Recombinant MYDGF therapy reversed these deficits. Liquid chromatography mass spectrometry analysis (LC-MS) analysis of cardiac ECM in Mydgf-KO mice revealed FGF1 as a critical downstream effector of Mydgf in angiogenesis. Administration of recombinant FGF1 protein significantly promoted endothelial cell proliferation and tube formation in human coronary artery endothelial cells. These findings establish the Mydgf-FGF1 axis as a critical regulator of cardiac angiogenesis and unveil its promise as a therapeutic target to promote vascular repair in ischemic heart disease.
Indexed as
Identifiers
40553382What OpenQuestion holds
Registered trials
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.