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Lecturer of Physiology at Optometry and Vision Sciences
Ask questions about Sumia A. Bageghni's research, publications, and ongoing work
Demonstrated that fibroblast-specific deletion of IL-1 receptor-1 reduces adverse cardiac remodeling following myocardial infarction, providing a potential therapeutic target.
Identified that cardiac fibroblast-specific p38α MAP kinase promotes cardiac hypertrophy via a paracrine interleukin-6 signaling mechanism, offering insights into hypertrophy mechanisms.
Showed that the nuclear matrix protein CIZ1 facilitates the localization of Xist RNA to the inactive X-chromosome territory, contributing to understanding X-chromosome inactivation.
Investigated the role of 11β-HSD1 in suppressing cardiac fibroblast activity and neutrophil recruitment after myocardial infarction.
Demonstrated that cardiomyocyte-specific expression of CIZ1 stimulates the production of mononucleated cells with an extended window of proliferation in the postnatal mouse heart.
Investigated inherent functional differences between human cardiac fibroblasts cultured from nondiabetic and Type 2 diabetic donors.
Investigated the role of MiR-214-3p in regulating Piezo1, lysyl oxidases and mitochondrial function in human cardiac fibroblasts.
Dr. Sumia Bageghni's research focuses on the cellular and molecular mechanisms of cardiovascular disease, particularly cardiac fibrosis and remodeling, with a focus on fibroblast biology and signaling pathways. Her work has contributed to understanding the role of specific proteins and pathways in heart disease.
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