What Is Vascular Endothelial Growth Factor (VEGF), and How Does It Support Hair Growth in Alopecia?

When we examine hair loss closely, one of the first questions we must ask is whether hair follicles are receiving the biological support they need to function. Vascular Endothelial Growth Factor, abbreviated as VEGF, is a protein produced naturally by the body that stimulates angiogenesis, the formation of new blood vessels from existing ones. Angiogenesis is essential because blood vessels deliver oxygen, glucose, amino acids, and hormones to tissues. Without sufficient blood supply, highly active tissues struggle to maintain normal function.

Hair follicles are among the most metabolically active structures in the skin during their growth phase. Metabolically active means they consume high amounts of energy. That energy depends on oxygen and nutrients transported through capillaries, the smallest blood vessels. VEGF acts by binding to specific receptors located on endothelial cells, which are the cells lining blood vessels. Once activated, these receptors trigger cellular division and migration, ultimately forming new vascular networks.

The biological role of VEGF is well established in cardiovascular medicine, oncology, and wound healing research, as documented extensively in biomedical databases such as PubMed and resources supported by the National Institutes of Health (NIH). Its relevance to hair biology emerged when researchers observed that VEGF levels fluctuate during the hair growth cycle.

VEGF Within the Hair Cycle: Evidence From Human and Animal Research

To understand whether VEGF genuinely supports hair growth, we must examine controlled studies rather than theoretical assumptions.

In 2001, Yano, Brown, and Detmar conducted a controlled experimental study published in The Journal of Clinical Investigation. The researchers genetically engineered mice to overexpress VEGF in their skin. The population consisted of laboratory mice, and the duration of observation extended through multiple hair cycles. Hair follicles were evaluated using histological analysis, meaning tissue samples were examined under a microscope to measure follicle size and surrounding blood vessel density.

The results demonstrated that mice with increased VEGF expression developed significantly larger hair follicles and denser perifollicular vasculature, which refers to blood vessels surrounding the hair follicle. Hair regrowth occurred more rapidly compared to control mice. The method of evaluation included microscopic measurement of follicular diameter and quantification of capillary density. However, the study’s limitation is fundamental: it was conducted in animals. Murine hair cycling differs from human hair cycling, and genetic overexpression models may not reflect typical clinical conditions such as androgenetic alopecia.

Human evidence was explored earlier by Lachgar et al. in 1998 in a study published in the British Journal of Dermatology. This research examined scalp biopsy samples obtained from patients undergoing hair transplantation procedures. The population consisted of adult human participants. The investigators used immunohistochemistry, a laboratory method that identifies specific proteins within tissue using antibodies, to measure VEGF expression during different phases of the hair cycle. The evaluation focused on comparing VEGF levels in follicles during anagen, the active growth phase, and telogen, the resting phase.

The researchers found that VEGF expression was significantly higher during anagen compared to telogen. This finding supports an association between VEGF activity and active hair growth. However, the study was observational and cross-sectional. It measured correlation rather than causation. It did not demonstrate that increasing VEGF alone would reverse alopecia.

Minoxidil and VEGF: Mechanistic Insights

If VEGF plays a supportive role in hair growth, we must ask whether approved treatments interact with this pathway. Minoxidil, an FDA-approved topical treatment for androgenetic alopecia, has been studied in this context.

In 2001, Li et al. published a mechanistic study in The Journal of Investigative Dermatology examining cultured human dermal papilla cells. Dermal papilla cells are specialized cells located at the base of the hair follicle that regulate hair growth and cycling. The researchers treated these cells with minoxidil in vitro, meaning in a** controlled laboratory environment outside the human body. They measured VEGF messenger RNA expression and protein production using molecular analysis techniques, including gene expression assays and protein quantification methods.**

The study demonstrated that minoxidil significantly increased VEGF production in dermal papilla cells. This provides a plausible biological explanation for part of minoxidil’s effect. Increased VEGF may enhance blood vessel formation around follicles, improving nutrient delivery during the growth phase. However,** this research was conducted in cell culture, not in living patients. In vitro studies do not account for systemic hormonal influences, immune responses, or long-term clinical outcomes.**

According to the U.S. Food and Drug Administration, minoxidil is approved for the treatment of androgenetic alopecia. The FDA’s approval is based on randomized clinical trials demonstrating increased hair counts compared to placebo. While these trials confirm clinical efficacy, they do not directly measure VEGF in patients, meaning VEGF’s contribution remains mechanistic rather than definitively proven in large-scale human trials.

VEGF in Androgenetic Alopecia: Supportive but Not Central

When evaluating alopecia, especially androgenetic alopecia, we must distinguish between primary causes and supportive biological processes. Androgenetic alopecia is primarily driven by dihydrotestosterone (DHT), a derivative of testosterone that binds to androgen receptors in genetically susceptible hair follicles. This binding leads to progressive miniaturization, meaning follicles shrink and produce thinner hairs over time.

Reduced perifollicular blood flow has been observed in balding scalp regions, suggesting vascular factors may contribute to disease progression. VEGF could theoretically counteract reduced circulation by promoting angiogenesis. However, current evidence does not demonstrate that VEGF deficiency is the primary driver of androgenetic alopecia. Instead, **VEGF appears to function as a supportive factor that enhances follicular performance when other inhibitory influences, such **as DHT sensitivity, are present.

This distinction is important. Increasing VEGF does not directly alter androgen receptor signaling or DHT production. Therefore, VEGF stimulation alone is unlikely to halt genetic pattern hair loss without addressing hormonal mechanisms.

Platelet-Rich Plasma and Growth Factors

Platelet-rich plasma (PRP) therapy has gained attention because platelets release multiple growth factors, including VEGF. A 2019 systematic review by Gupta and Carviel in Aesthetic Plastic Surgery evaluated clinical trials involving PRP for androgenetic alopecia. The review analyzed several small randomized and controlled human studies with treatment durations ranging from three to six months. Evaluation methods typically included hair counts using dermoscopy, standardized photography, and patient self-assessment questionnaires.

Many studies reported increases in hair density and thickness. However, the review emphasized limitations such as small sample sizes, lack of standardized preparation protocols, short follow-up periods, and variability in injection techniques. Importantly, PRP contains multiple growth factors, making it impossible to isolate the specific contribution of VEGF.

As of current FDA documentation, PRP is not specifically approved as a treatment for hair loss. Its clinical evidence remains suggestive but not definitive.

What Do We Need to Understand About VEGF and Hair Growth?

When we critically evaluate the research, several conclusions emerge. VEGF clearly participates in the biological environment of active hair growth. Animal studies demonstrate that artificially increasing VEGF enhances follicle size and vascular density. Human tissue studies confirm that VEGF expression peaks during the growth phase of the hair cycle. Laboratory research shows that minoxidil stimulates VEGF production in dermal papilla cells.

However, there is limited high-quality, large-scale, long-duration randomized clinical evidence in humans demonstrating that directly increasing VEGF alone reverses alopecia. Much of the evidence is mechanistic, preclinical, or based on small trials. VEGF appears to be a facilitator of hair growth rather than a primary driver of hair loss pathology.

Therefore, if we are asking whether VEGF supports hair growth in alopecia, the answer is yes in a supportive biological sense. It enhances vascular supply, which is necessary for active follicular function. Yet it does not replace treatments that address the central hormonal mechanisms underlying androgenetic alopecia.

A clear understanding requires recognizing both the biological plausibility and the limitations of current evidence.

References

Gupta, A. K., & Carviel, J. L. (2019). Platelet-rich plasma for androgenetic alopecia: A systematic review. Aesthetic Plastic Surgery, 43(6), 1421–1431. https://pubmed.ncbi.nlm.nih.gov/31098833/

Lachgar, S., Charvéron, M., Gall, Y., & Bonafé, J. L. (1998). Expression of vascular endothelial growth factor in human hair follicle during hair cycle. British Journal of Dermatology, 138(3), 407–411. https://pubmed.ncbi.nlm.nih.gov/9580791/

Li, M., Marubayashi, A., Nakaya, Y., Fukui, K., & Arase, S. (2001). Minoxidil-induced hair growth is mediated by adenosine in cultured dermal papilla cells: Possible involvement of vascular endothelial growth factor. Journal of Investigative Dermatology, 117(6), 1594–1600. https://pubmed.ncbi.nlm.nih.gov/11886508/

National Institutes of Health. (n.d.). Vascular endothelial growth factor (VEGF). National Library of Medicine. https://www.ncbi.nlm.nih.gov/

U.S. Food and Drug Administration. (n.d.). Orange Book: Approved drug products with therapeutic equivalence evaluations. https://www.accessdata.fda.gov/scripts/cder/ob/

Yano, K., Brown, L. F., & Detmar, M. (2001). Control of hair growth and follicle size by VEGF-mediated angiogenesis. Journal of Clinical Investigation, 107(4), 409–417. https://pubmed.ncbi.nlm.nih.gov/11181641/