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Stefan E. Hardt

Researcher at Heidelberg University

Publications -  112
Citations -  9702

Stefan E. Hardt is an academic researcher from Heidelberg University. The author has contributed to research in topics: Heart failure & Coronary artery disease. The author has an hindex of 35, co-authored 105 publications receiving 8354 citations. Previous affiliations of Stefan E. Hardt include Rutgers University & University Hospital Heidelberg.

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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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High-Mobility Group Box-1 in Ischemia-Reperfusion Injury of the Heart

TL;DR: It is demonstrated that HMGB1 acts as an early mediator of inflammation and organ damage in I/R injury of the heart by binding to RAGE, resulting in the activation of proinflammatory pathways and enhanced myocardial injury.
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Glycogen synthase kinase-3beta: a novel regulator of cardiac hypertrophy and development.

TL;DR: The role of GSK-3β in cardiac hypertrophy and development and the potential underlying mechanisms are discussed in this article, where the authors show that GSK3β is an essential negative regulator of cardiac hyper-trophy.
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Longitudinal Left Ventricular Function for Prediction of Survival in Systemic Light-Chain Amyloidosis: Incremental Value Compared With Clinical and Biochemical Markers

TL;DR: In the largest serial investigation reported so far, reduced LV longitudinal function served as an independent predictor of survival in AL amyloidosis and offered incremental information beyond standard clinical and serological parameters.
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Glycogen Synthase Kinase 3β Regulates GATA4 in Cardiac Myocytes

TL;DR: Results suggest that GSK3β negatively regulates nuclear expression of GATA4 by stimulating Crm1-dependent nuclear export, which may represent an important signaling mechanism mediating cardiac hypertrophy.