Mahnaz Shariatzadeh

Post doc

Mahnaz Shariatzadeh investigates how enhancing O-GlcNAcylation may protect the failing heart, preserve cardiac function, and improve metabolic resilience during acute cardiac stress. Her research focuses on the molecular mechanisms underlying metabolic adaptation and maladaptation in acute decompensated heart failure (ADHF), with the aim of identifying pathways that could be targeted to improve cardiac responses to acute decompensation. This research is conducted within the ERA4Health CARDINNOV GANDHI project, an international collaborative initiative aimed at identifying novel therapeutic targets for heart failure. To investigate these mechanisms across multiple levels of cardiac biology, Mahnaz combines complementary experimental platforms, including in vitro models of acute heart failure based on primary animal cardiomyocytes, human stem cell-derived cardiomyocytes, and engineered heart tissue (EHT). Together, these models allow her to examine the effects of O-GlcNAcylation across molecular and cellular pathways as well as tissue-level cardiac function, while providing increasingly physiologically relevant systems for validating experimental findings.

By integrating molecular, metabolic, and functional approaches, Mahnaz aims to bridge fundamental mechanistic insights with translational applications. This work seeks to determine whether modulation of O-GlcNAcylation can enhance the ability of the failing heart to adapt to metabolic stress and ultimately contribute to the development of new therapeutic strategies for ADHF.