Renata O. Pereira

ATF4‐dependent increase in mitochondrial‐endoplasmic reticulum tethering following OPA1 deletion in skeletal muscle

Systematic Transmission Electron Microscopy‐Based Identification and 3D Reconstruction of Cellular Degradation Machinery

A Comprehensive Approach to Sample Preparation for Electron Microscopy and the Assessment of Mitochondrial Morphology in Tissue and Cultured Cells

A Universal Approach to Analyzing Transmission Electron Microscopy with ImageJ

Maintaining Myocardial Glucose Utilization in Diabetic Cardiomyopathy Accelerates Mitochondrial Dysfunction

Mitochondrial Reactive Oxygen Species in Lipotoxic Hearts Induce Post-Translational Modifications of AKAP121, DRP1, and OPA1 That Promote Mitochondrial Fission

<scp>OPA</scp> 1 deficiency promotes secretion of <scp>FGF</scp> 21 from muscle that prevents obesity and insulin resistance

Insulin Receptor Substrates Are Essential for the Bioenergetic and Hypertrophic Response of the Heart to Exercise Training

Enhanced Cardiac Akt/Protein Kinase B Signaling Contributes to Pathological Cardiac Hypertrophy in Part by Impairing Mitochondrial Function via Transcriptional Repression of Mitochondrion-Targeted Nuclear Genes

Maintaining PGC‐1α expression following pressure overload‐induced cardiac hypertrophy preserves angiogenesis but not contractile or mitochondrial function

GLUT1 deficiency in cardiomyocytes does not accelerate the transition from compensated hypertrophy to heart failure

Insulin receptor substrate signaling suppresses neonatal autophagy in the heart

Inducible Overexpression of GLUT1 Prevents Mitochondrial Dysfunction and Attenuates Structural Remodeling in Pressure Overload but Does Not Prevent Left Ventricular Dysfunction

The absence of insulin signaling in the heart induces changes in potassium channel expression and ventricular repolarization

Cardiac PI3K-Akt Impairs Insulin-Stimulated Glucose Uptake Independent of mTORC1 and GLUT4 Translocation