생화학분자생물학회

	Anthony Mukwaya ( Anthonny.mukwaya@liu.se )
	2018-present	Principal research engineer/scientist, linkoping University, Sweden
	2014-2018	PhD in medical sciences, linkoping University, Sweden
	2012-2013	Master of science molecular biology and biotechnology, University of Skovde, Sweden
	2005-2008	Bachelor of Biomedical Laboratory Technology, Makerere University, Ugandac

Relapse of pathological angiogenesis: functional role of the basement membrane and potential treatment strategies

Blinding eye diseases such as corneal neovascularization, proliferative diabetic retinopathy, and age-related macular degeneration are driven by pathological angiogenesis. In cancer, angiogenesis is key for tumor growth and metastasis. Current antiangiogenic treatments applied clinically interfere with the VEGF signaling pathway-the main angiogenic pathway-to inhibit angiogenesis. These treatments are, however, only partially effective in regressing new pathologic vessels, and the disease relapses following cessation of treatment. Moreover, the relapse of pathological angiogenesis can be rapid, aggressive and more difficult to treat than angiogenesis in the initial phase. The manner in which relapse occurs is poorly understood; however, recent studies have begun to shed light on the mechanisms underlying the revascularization process. Hypotheses have been generated to explain the rapid angiogenic relapse and increased resistance of relapsed disease to treatment. In this context, the present review summarizes knowledge of the various mechanisms of disease relapse gained from different experimental models of pathological angiogenesis. In addition, the basement membrane-a remnant of regressed vessels-is examined in detail to discuss its potential role in disease relapse. Finally, approaches for gaining a better understanding of the relapse process are discussed, including prospects for the management of relapse in the context of disease.


Exp Mol Med. 2021 Feb 15. doi: 10.1038/s12276-021-00566-2.
https://pubmed.ncbi.nlm.nih.gov/33589713/