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Cissy Chenyi Zhou

Researcher at University of Texas Health Science Center at Houston

Publications -  9
Citations -  1193

Cissy Chenyi Zhou is an academic researcher from University of Texas Health Science Center at Houston. The author has contributed to research in topics: Preeclampsia & Angiotensin receptor. The author has an hindex of 8, co-authored 9 publications receiving 1086 citations. Previous affiliations of Cissy Chenyi Zhou include University of Birmingham & Texas A&M Health Science Center.

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Angiotensin receptor agonistic autoantibodies induce pre-eclampsia in pregnant mice

TL;DR: It is shown that key features of pre-eclampsia, including hypertension, proteinuria, glomerular endotheliosis, placental abnormalities and small fetus size appeared in pregnant mice after injection with either total IgG or affinity-purified AT1-AAs from women with pre- eclampsIA.
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Autoantibody from women with preeclampsia induces soluble Fms-like tyrosine kinase-1 production via angiotensin type 1 receptor and calcineurin/nuclear factor of activated T-cells signaling

TL;DR: These studies demonstrate that an autoantibody from women with preeclampsia induces sFlt-1 production via angiotensin receptor activation and downstream calcineurin/nuclear factor of activated T-cells signaling, which represent potentially important targets for diagnosis and therapeutic intervention.
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Angiotensin II Induces Soluble fms-Like Tyrosine Kinase-1 Release via Calcineurin Signaling Pathway in Pregnancy

TL;DR: It is reported that infusion of Ang II significantly increases circulating levels of sFlt-1 in pregnant mice, thereby demonstrating that Ang II is a regulator of sMaternal endothelial cell migration and in vitro tube formation and revealing a previously unrecognized regulatory role for Ang II on sFelt-1 expression in murine and human pregnancy.
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Angiotensin Receptor Agonistic Autoantibody–Mediated Tumor Necrosis Factor-α Induction Contributes to Increased Soluble Endoglin Production in Preeclampsia

TL;DR: It is demonstrated that AT1-AA–mediated tumor necrosis factor-&agr; induction, by overcoming its negative regulator, heme oxygenase-1, is a key underlying mechanism responsible for impaired placental angiogenesis by inducing both sEng and soluble fms-like tyrosine kinase- 1 secretion from human villous explants.
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Autoantibody-Mediated IL-6–Dependent Endothelin-1 Elevation Underlies Pathogenesis in a Mouse Model of Preeclampsia

TL;DR: Human and mouse studies are provided showing that angiotensin II type I receptor-agonistic autoantibody is a novel causative factor responsible for elevated ET-1 production and that increased TNF-α/IL-6 signaling is a key mechanism underlying increased ET- 1 production and subsequent maternal features.