Wei Ruan

May 29, 2024 | digitalcommons.library.tmc.edu | Wei Ruan |Xinxin Ma |Yafen Liang |Jochen Daniel Muehlschlegel

Home > UTHealth > McGovern Medical School > Journal Articles > 795 A2A, A2B, Adora2a, Adora2b, CD39, CD73, ENT1, ENT2, adenosine, hypoxia DOWNLOADS COinS

Dec 20, 2023 | nature.com | Xiaoyi Yuan |Wei Ruan |Peter Carmeliet

AbstractHypoxia-inducible factors (HIFs) are highly conserved transcription factors that are crucial for adaptation of metazoans to limited oxygen availability. Recently, HIF activation and inhibition have emerged as therapeutic targets in various human diseases. Pharmacologically desirable effects of HIF activation include erythropoiesis stimulation, cellular metabolism optimization during hypoxia and adaptive responses during ischaemia and inflammation.

Jul 3, 2023 | nature.com | Wei Ruan |Holger K. Eltzschig |Xiaoyi Yuan

The PHD–pVHL pathway is essential for oxygen-dependent prolyl hydroxylation of HIFA. A recent study identifies RIPK1 as a hydroxylation target in this pathway during hypoxia-induced cell death and presents a 2.8 Å resolution crystal structure of the pVHL–elongin B/C complex bound to hydroxylated RIPK1. Zhang et al.6 began by exploring the functional role of RIPK1 in hypoxia-induced cell death.

Jun 8, 2023 | insight.jci.org | JCI Insight |Wei Ruan |Jiwen Li |Seungwon Choi

AbstractPrevious studies implicate extracellular adenosine signaling in attenuating myocardial ischemia and reperfusion injury (IRI). This extracellular adenosine signaling is terminated by its uptake into cells by equilibrative nucleoside transporters (ENTs). Thus, we hypothesized that targeting ENTs would function to increase cardiac adenosine signaling and concomitant cardioprotection against IRI. Mice were exposed to myocardial ischemia and reperfusion injury.

Jun 8, 2023 | digitalcommons.library.tmc.edu | Wei Ruan |Jiwen Li |Seungwon Choi |Xinxin Ma

Previous studies implicate extracellular adenosine signaling in attenuating myocardial ischemia and reperfusion injury (IRI). This extracellular adenosine signaling is terminated by its uptake into cells by equilibrative nucleoside transporters (ENTs). Thus, we hypothesized that targeting ENTs would function to increase cardiac adenosine signaling and concomitant cardioprotection against IRI. Mice were exposed to myocardial ischemia and reperfusion injury.