Anti-Apoptotic Protein BCL-xL Inhibitors as Potential Treatment for Retinal Neovascularization

Article: Discovery of a new drug for diabetic retinopathy
Source: University of Montreal (Canada), via EyeNet
Published: February 11, 2021

Healthy and pathological retinal vascularization

Understanding the molecular basis of angiogenesis is a foundation to developing therapies for eye diseases due to abnormal neovascularization, eye diseases such as diabetic retinopathy. A team of researchers in Canada and the U.S. discovered that in contrast to healthy blood vessels, pathological blood vessels engage in pathways of cellular senescence, or accelerated aging. They then induced senolysis, the selective destruction of senescent cells, by either genetically eliminating the senescent cells (specifically p16^INK4A-expressing cells) or by using small molecule inhibitors of the anti-apoptotic protein BCL-xL. BCL-xL is a molecular target present in defective blood vessels. Senolysis was found to suppress pathological angiogenesis, consequently providing a better environment for physiological vascular repair. As the news article states, Phase 1 clinical trials are underway to test the potential of this new class of drug for treatment of diseases of retinal neovascularization.

Personal commentary: Note that this article is from February of this year. I think I had skipped it in the early days of the blog while I decided what kinds of articles to include or comment about. Back then, I hadn't expanded to taking a closer look at the research journal article. The news article from the University of Montreal in this case is on the simpler side, probably contributing to its exclusion from commentary initially. But upon a second round of review, it is still a science news article about eyes, especially from an academic/university news source. So minor commentary is included here.

My rating of this study: ⭐⭐

Crespo-Garcia S, Tsuruda PR, Dejda A, et al. "Pathological angiogenesis in retinopathy engages cellular senescence and is amenable to therapeutic elimination via BCL-xL inhibition." Cell Metabolism. 5 February 2021. https://doi.org/10.1016/j.cmet.2021.01.011