Athenea Perez-Serna

Athenea Perez-Serna
Universidad Miguel Hernández de Elche | UMH · Department of Phisiology

Cellular and Molecular Biology PhD student
Estrogen effects on pancreatic islets and beta cells under proapoptotic stress.

About

3
Publications
172
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9
Citations
Introduction
PhD candidate at Dept. of Basic Diabetes Research in UMH under leadership of Dr. Laura Marroquí and Dr. Ángel Nadal. My research project focuses on the impact of xenoestrogenic endocrine disruptors in pancreatic beta cell survival and function. We aim to study the effects of these chemicals in Type 1 Diabetes pathogenesis and progression
Additional affiliations
September 2020 - present
Universidad Miguel Hernández de Elche
Position
  • PhD Student
Description
  • I am a PhD candidate at UMH under the supervision of Dr. Laura Marroquí and Dr. Ángel Nadal. My research focuses on the impact of endocrine disruptors in pancreatic beta-cell survival under type 1 diabetes (T1D) conditions. In the last decades, incidence of T1D has greatly increased. Nowadays, genetic factors have a smaller role in T1D, with a more important contribution from environmental insults. We aim to understand the role of endocrine disruptors in the beta-cell apoptosis at T1D onset.
August 2019 - July 2020
Universidad Miguel Hernández de Elche
Position
  • Research Assistant
Education
July 2020 - August 2024
Universidad Miguel Hernández de Elche
Field of study
  • Molecular and Cellular Biology - Diabetes Research
July 2019 - June 2020
Universidad Miguel Hernández de Elche
Field of study
  • Biotechnology and Bioengineering
September 2012 - June 2019
Universidad Miguel Hernández de Elche
Field of study
  • Biotechnology

Publications

Publications (3)
Article
17β-estradiol protects pancreatic β-cells from apoptosis via the estrogen receptors ERα, ERβ and GPER. Conversely, the endocrine disruptor bisphenol-A (BPA), which exerts multiple effects in this cell type via the same estrogen receptors, increased basal apoptosis. The molecular-initiated events that trigger these opposite actions have yet to be id...
Preprint
17β-estradiol protects pancreatic β-cells from apoptosis via the estrogen receptors ERα, ERβ and GPER. Conversely, the endocrine disruptor Bisphenol-A (BPA), which exerts multiple effects in this cell type via the same estrogen receptors, increased basal apoptosis. The molecular initiated events that trigger these opposite actions have yet to be id...
Chapter
Type 1 diabetes (T1D) is a chronic autoimmune disease characterized by pancreatic islet inflammation (insulitis) and specific pancreatic β-cell destruction by an immune attack. Although the precise underlying mechanisms leading to the autoimmune assault remain poorly understood, it is well accepted that insulitis takes place in the context of a con...

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