The nitty-gritty of vascular permeability in cancer: targeting blood endothelium to control metastases.
Level 5 - mechanism / opinion, no new human data
Narrative review detailing biological mechanisms without systematic methodology or original human data.
PubMed 42252654 · doi:10.1111/bph.70505
What was done
This narrative review synthesised literature on the structural and molecular determinants of cancer-associated blood vascular permeability, focusing on paracellular leakage via endothelial tight junctions, adherens junctions, and the glycocalyx. It evaluated how microenvironmental cues (such as hypoxia, mechanical stress, and VEGF-driven Src/VE-cadherin signalling) induce chronic vascular hyperpermeability and discussed pharmacological strategies designed to retighten the endothelial barrier.
What was found
No quantitative data or empirical findings are reported in the abstract. The review presents a mechanistic framework arguing that vascular hyperpermeability actively promotes intravasation, extravasation, and metastatic niche formation, and contends that restoring endothelial barrier function could inhibit metastasis.
Why it matters
The review outlines an alternative paradigm to traditional anti-angiogenic vascular ablation, proposing that pharmacological barrier restoration is an underexploited approach to impede metastatic spread.
Limits
As a non-systematic narrative review, it contains no new human data, clinical trials, or quantitative synthesis. The clinical efficacy and safety of selectively modulating endothelial barrier integrity to prevent metastasis remain unproven.
Cited by
- supports Cancer utilizes vascular endothelial growth factor (VEGF) to establish blood supply and facilitate metastasis from primary tumors.