Yalu Zhou

VEGFA-Positive Macrophages Regulate Aqueous Humor Outflow in Aged Mice and Humans

This study identifies VEGFA-producing macrophages around Schlemm's canal as a compensatory mechanism maintaining aqueous humor outflow during aging and vascular stress, suggesting TIE2 activation as a therapeutic target.

Endothelial Prolyl Hydroxylase 3 Mitigates Maladaptive Inflammation to Promote Post-Ischemic Kidney Repair

This study identifies endothelial PHD3 as a regulator of kidney repair after ischemia, showing its role in suppressing inflammation and fibrosis through HIF-dependent mechanisms.

The transcription factor TCF21 is necessary for adoption of cell fates by Foxd1+ stromal progenitors during kidney development

This study uses scRNA-seq to show that Tcf21 is essential for Foxd1+ stromal progenitor differentiation during kidney development, with loss of Tcf21 causing stromal subpopulation depletion and emergence of Emcn-expressing cells.

Piezo1 Triggers an Angiopoietin-2-Integrin Signaling Loop in Schlemm's Canal to Regulate Intraocular Pressure

The paper identifies a PIEZO1-ANGPT2-ITGA9 signaling pathway in Schlemm's canal endothelium that regulates intraocular pressure and glaucoma.

Targeting CHEK2-YBX1&YBX3 regulatory hub to potentiate immune checkpoint blockade response in gliomas

This study identifies the CHK2-YBX1&YBX3 hub as an immunosuppressive mechanism in gliomas and shows that targeting it with SU056 enhances immune checkpoint blockade efficacy.

Immunomodulatory Role of the Stem Cell Circadian Clock in Muscle Repair

This study shows that the circadian clock in muscle stem cells modulates immune responses and inflammation during muscle regeneration through NAD+ metabolism and CCL2 signaling.

Post-ischemic inactivation of HIF prolyl hydroxylases in endothelium promotes maladaptive kidney repair by inducing glycolysis

This study shows that inactivating PHD enzymes in endothelial cells after ischemic kidney injury promotes maladaptive repair through glycolysis and MCT4, which can be reversed by MCT4 inhibitors.

Chemical inhibition of prolyl hydroxylases impairs angiogenic competence of human vascular endothelium through metabolic reprogramming

This study shows that inhibiting prolyl hydroxylases with DMOG impairs angiogenic competence of human vascular endothelial cells through metabolic reprogramming.