Definition
- Similarly, myokines, such as VEGF and FGF2, are released from the muscle to promote the formation of new blood vessels in the muscle itself, thereby improving endurance capacity PMID 40869331
- This identification revealed VEGF as a potent endothelial mitogen with high specificity, further confirmed by studies on its role in vascular permeability and EC proliferation. PMID 40383803
Biological function
- Promotes formation of new blood vessels in skeletal muscle to improve endurance capacity PMID 40869331
- Central factor in initiating angiogenesis PMID 34606978
- Vascular endothelial growth factor (VEGF) signaling is a critical regulator of vasculogenesis, angiogenesis, and lymphangiogenesis, processes that are vital for the development of vascular and lymphatic systems, tissue repair, and the maintenance of homeostasis. PMID 40383803
- The VEGF family, comprising VEGF-A, VEGF-B, VEGF-C, and VEGF-D, regulates vascular and lymphatic development through isoforms generated by alternative splicing20 or proteolytic cleavage. PMID 40383803
- Specifically, the signaling axis of VEGF-VEGFR controls endothelial cell (EC) proliferation, migration, and survival, thereby facilitating the organized development of new blood vessels. PMID 40383803
Exerkine classification
- Long-term + short-term exercise upregulates VEGF signaling and capillarity in skeletal muscles PMID 34606978
- Exercise showed increased VEGF mRNA and protein levels PMID 34606978
- Acute exercise in animals increases AMPRK to stimulate VEGF mRNA levels PMID 37964253
Therapeutic potential
- Recent studies have identified exerkines, which are secreted from multiple tissues in response to exercise, as major players in orchestrating cell-to-cell crosstalk and mediating the exercise-induced beneficial effects. PMID 34606978
- The growth of functional capillaries following exercise is the result of increases in proangiogenic factors, among which VEGF signaling plays a crucial role. PMID 34606978
- VEGF-targeted therapies, such as monoclonal antibodies and tyrosine kinase inhibitors, have revolutionized the treatment of diseases involving pathological angiogenesis, offering significant clinical benefits in oncology and ophthalmology PMID 40383803
- Intracoronary VEGF-A gene transfer improves myocardial perfusion, offering a strategy for therapeutic angiogenesis in ischemic heart disease. PMID 40383803
- Exogenous VEGF-A mitigates hypoglycemia-induced damage, suggesting potential therapeutic applications. PMID 40383803
- The diverse roles of VEGF ligands and their receptors drive pathological processes, including tumor angiogenesis, cardiovascular diseases, ocular diseases, and metabolic/immune-related/reproductive disorders. Key molecular interactions and downstream signaling pathways are upregulated or dysregulated in disease states, thereby promoting cell survival, migration, and proliferation. These pathways highlight the therapeutic potential of targeting VEGF/VEGFR signaling across various disease contexts. ATH atherosclerosis, MI myocardial ischemia, DR diabetic retinopathy, AMD age-related macular degeneration, FA fatty acid, NAFLD non-alcoholic fatty liver disease, RA rheumatoid arthritis, PE pre-eclampsia, EM endometriosis PMID 40383803
- FGF21 also increased VEGF expression , and intramuscular injection of Ad-FGF21 increased capillary density in post-MI hearts PMID 37535710
Evidence
27,809PubMed publications, last 5 years#3 of 35
43%Mention “therapeutic” or “therapy”12,059 publications
3,909Registered clinical trials#3 of 35
792Active or recruiting trials
Therapeutic mentionOther
Early phase 1 · 58Phase 1 · 756Phase 2 · 1,481Phase 3 · 374Phase 4 · 248Not applicable · 716
PubMed and ClinicalTrials.gov, snapshot of February 2026. Counts are keyword-based and include every study that mentions VEGF. Compare across exerkines →
References 5
Primary literature cited in this profile. Each identifier opens the article on PubMed.