Sökning: id:"swepub:oai:DiVA.org:liu-173902" >
Relapse of patholog...
-
Mukwaya, AnthonnyLinköpings universitet,Avdelningen för sinnesorgan och kommunikation,Medicinska fakulteten
(författare)
Relapse of pathological angiogenesis : functional role of the basement membrane and potential treatment strategies
- Artikel/kapitelEngelska2021
Förlag, utgivningsår, omfång ...
-
2021-02-15
-
Springer Nature,2021
-
electronicrdacarrier
Nummerbeteckningar
-
LIBRIS-ID:oai:DiVA.org:liu-173902
-
https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-173902URI
-
https://doi.org/10.1038/s12276-021-00566-2DOI
Kompletterande språkuppgifter
-
Språk:engelska
-
Sammanfattning på:engelska
Ingår i deldatabas
Klassifikation
-
Ämneskategori:ref swepub-contenttype
-
Ämneskategori:for swepub-publicationtype
Anmärkningar
-
Funding Agencies|Ogonfonden, from the charity Synskadades Val; Swedish society of ophthalmology; Linkoping University
-
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. Blood vessel formation: understanding relapse after inhibitory treatment Studying the sites of previous blood vessel occupation may explain how pathological vessel growth recurs after inhibitory treatment. Angiogenesis, the growth of new blood vessels, drives progression of cancerous tumors and blinding eye diseases. Existing treatments inhibiting critical growth factors are effective in the short term, but are often followed by aggressive relapse. Mukwaya et al., from Linkoping University in Sweden review the role of empty basement membrane sleeves (EBMS), the remnants of regressed blood vessels. Basement membrane supports endothelial cells, and EBMS could act as a scaffold for endothelial cells to rapidly rebuild blood vessels after anti-angiogenic treatment. Alternatively, EBMS may represent irreversibly abandoned conduits permanently isolated from the circulation, putatively through the deposition of excess collagen. Future work should carefully examine the role of basement membrane in the relapse of pathologic vessel growth.
Ämnesord och genrebeteckningar
Biuppslag (personer, institutioner, konferenser, titlar ...)
-
Jensen, LasseLinköpings universitet,Avdelningen för diagnostik och specialistmedicin,Medicinska fakulteten,Region Östergötland, Klinisk farmakologi(Swepub:liu)larje86
(författare)
-
Lagali, NeilLinköpings universitet,Avdelningen för sinnesorgan och kommunikation,Medicinska fakulteten,Region Östergötland, Ögonkliniken US,Sorlandet Hosp Arendal, Norway(Swepub:liu)neina50
(författare)
-
Linköpings universitetAvdelningen för sinnesorgan och kommunikation
(creator_code:org_t)
Sammanhörande titlar
-
Ingår i:Experimental and Molecular Medicine: Springer Nature53, s. 189-2011226-36132092-6413
Internetlänk
Hitta via bibliotek
Till lärosätets databas