AI Article Synopsis
- The review examines the function of kallikrein-related peptidase 3 (KLK3), or prostate-specific antigen (PSA), in angiogenesis regulation.
- Initial research indicates that KLK3 can inhibit angiogenesis, likely due to its proteolytic activity.
- Recent findings propose that KLK3 might also promote angiogenesis by activating vascular endothelial growth factors VEGF-C and VEGF-D.
Article Abstract
In this focused review, we address the role of the kallikrein-related peptidase 3 (KLK3), also known as prostate-specific antigen (PSA), in the regulation of angiogenesis. Early studies suggest that KLK3 is able to inhibit angiogenic processes, which is most likely dependent on its proteolytic activity. However, more recent evidence suggests that KLK3 may also have an opposite role, mediated by the ability of KLK3 to activate the (lymph)angiogenic vascular endothelial growth factors VEGF-C and VEGF-D, further discussed in the review.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8704207 | PMC |
| http://dx.doi.org/10.3390/ijms222413545 | DOI Listing |
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