Reduced Endoglin Activity Limits Cardiac Fibrosis and Improves Survival in Heart Failure | Zendy

Navin K. Kapur | Zendy; Szuhuei Wilson | Zendy; Adil Yunis | Zendy; Xiaoying Qiao | Zendy; Emily Mackey | Zendy; Vikram Paruchuri | Zendy; Corey Baker | Zendy; Mark Aronovitz | Zendy; S. Ananth Karumanchi | Zendy; Michelle Letarte | Zendy; David A. Kass | Zendy; Michael E. Mendelsohn | Zendy; Richard H. Karas | Zendy

AI Assistant Blog Pricing

Home ZAIA Blog

Open Access

Reduced Endoglin Activity Limits Cardiac Fibrosis and Improves Survival in Heart Failure

Author(s) -

Navin K. Kapur,

Szuhuei Wilson,

Adil Yunis,

Xiaoying Qiao,

Emily Mackey,

Vikram Paruchuri,

Corey Baker,

Mark Aronovitz,

S. Ananth Karumanchi,

Michelle Letarte,

David A. Kass,

Michael E. Mendelsohn,

Richard H. Karas

Publication year - 2012

Publication title -

circulation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 7.795

H-Index - 607

eISSN - 1524-4539

pISSN - 0009-7322

DOI - 10.1161/circulationaha.111.080002

Subject(s) - endoglin , heart failure , medicine , cardiac fibrosis , fibrosis , ventricle , transforming growth factor , ventricular remodeling , cardiac function curve , cardiology , microbiology and biotechnology , biology , stem cell , cd34

Heart failure is a major cause of morbidity and mortality worldwide. The ubiquitously expressed cytokine transforming growth factor-β1 (TGFβ1) promotes cardiac fibrosis, an important component of progressive heart failure. Membrane-associated endoglin is a coreceptor for TGFβ1 signaling and has been studied in vascular remodeling and preeclampsia. We hypothesized that reduced endoglin expression may limit cardiac fibrosis in heart failure.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research