Nature Communications (Jul 2022)
Cardiac disruption of SDHAF4-mediated mitochondrial complex II assembly promotes dilated cardiomyopathy
- Xueqiang Wang,
- Xing Zhang,
- Ke Cao,
- Mengqi Zeng,
- Xuyang Fu,
- Adi Zheng,
- Feng Zhang,
- Feng Gao,
- Xuan Zou,
- Hao Li,
- Min Li,
- Weiqiang Lv,
- Jie Xu,
- Jiangang Long,
- Weijin Zang,
- Jinghai Chen,
- Jian Ding,
- Jiankang Liu,
- Zhihui Feng
Affiliations
- Xueqiang Wang
- School of Health and Life Sciences, University of Health and Rehabilitation Sciences
- Xing Zhang
- Key Laboratory of Aerospace Medicine of the Ministry of Education, School of Aerospace Medicine, Fourth Military Medical University
- Ke Cao
- Center for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi’an Jiaotong University
- Mengqi Zeng
- Center for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi’an Jiaotong University
- Xuyang Fu
- Department of Cardiology, Provincial Key Lab of Cardiovascular Research, Second Affiliated Hospital, Zhejiang University School of Medicine
- Adi Zheng
- Center for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi’an Jiaotong University
- Feng Zhang
- Department of Cardiology, Provincial Key Lab of Cardiovascular Research, Second Affiliated Hospital, Zhejiang University School of Medicine
- Feng Gao
- Department of Cardiology, Provincial Key Lab of Cardiovascular Research, Second Affiliated Hospital, Zhejiang University School of Medicine
- Xuan Zou
- National & Local Joint Engineering Research Center of Biodiagnosis and Biotherapy, The Second Affiliated Hospital of Xi’an Jiaotong University
- Hao Li
- Center for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi’an Jiaotong University
- Min Li
- Key Laboratory of Aerospace Medicine of the Ministry of Education, School of Aerospace Medicine, Fourth Military Medical University
- Weiqiang Lv
- Center for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi’an Jiaotong University
- Jie Xu
- Center for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi’an Jiaotong University
- Jiangang Long
- Center for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi’an Jiaotong University
- Weijin Zang
- Department of Pharmacology, School of Basic Medical Sciences, Xi’an Jiaotong University Health Science Center
- Jinghai Chen
- Department of Cardiology, Provincial Key Lab of Cardiovascular Research, Second Affiliated Hospital, Zhejiang University School of Medicine
- Jian Ding
- Center for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi’an Jiaotong University
- Jiankang Liu
- School of Health and Life Sciences, University of Health and Rehabilitation Sciences
- Zhihui Feng
- School of Health and Life Sciences, University of Health and Rehabilitation Sciences
- DOI
- https://doi.org/10.1038/s41467-022-31548-1
- Journal volume & issue
-
Vol. 13,
no. 1
pp. 1 – 16
Abstract
Functional succinate dehydrogenase (SDH) complex is vital to mitochondrial homeostasis. Here the authors show that disruption of SDH assembly in the heart causes dilated cardiomyopathy via impairing the mitochondrial integrity and metabolism and that mitochondrial interventions can be an effective approach to ameliorate the disease progression.
