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Uncompensated mitochondrial oxidative stress underlies heart failure in an iPSC-derived model of congenital heart disease

Xinxiu Xu, Kang Jin, Abha Bais, Wenjuan Zhu, Hisato Yagi, Timothy N. Feinstein, Phong K. Nguyen, Joseph D. Criscione, Xiaoqin Liu, Gisela Beutner, Kalyani B. Karunakaran, Krithika Rao, Haoting He, Phillip S. Adams, Catherine K. Kuo, Dennis Kostka, Gloria Pryhuber, Sruti Shiva, Madhavi K. Ganapathiraju, George A. Porter, Jiuann‐Huey Lin, Bruce J. Aronow, Cecilia Lo

2022Cell stem cell85 citationsDOIOpen Access PDF

Topics & Concepts

Oxidative stressMitochondrial permeability transition poreHeart failureBiologyEndoplasmic reticulumMitochondrionHeart diseaseUnfolded protein responseInduced pluripotent stem cellInternal medicineMitochondrial diseaseMPTPApoptosisEndocrinologyCardiologyDiseaseCell biologyProgrammed cell deathMedicineEmbryonic stem cellParkinson's diseaseBiochemistryMitochondrial DNAGeneMitochondrial Function and PathologyCongenital heart defects researchCongenital Heart Disease Studies
Uncompensated mitochondrial oxidative stress underlies heart failure in an iPSC-derived model of congenital heart disease | Litcius