Nature Communications (Mar 2023)
A defect in mitochondrial protein translation influences mitonuclear communication in the heart
- Feng Gao,
- Tian Liang,
- Yao Wei Lu,
- Xuyang Fu,
- Xiaoxuan Dong,
- Linbin Pu,
- Tingting Hong,
- Yuxia Zhou,
- Yu Zhang,
- Ning Liu,
- Feng Zhang,
- Jianming Liu,
- Andrea P. Malizia,
- Hong Yu,
- Wei Zhu,
- Douglas B. Cowan,
- Hong Chen,
- Xinyang Hu,
- John D. Mably,
- Jian’an Wang,
- Da-Zhi Wang,
- Jinghai Chen
Affiliations
- Feng Gao
- Department of Cardiology, Provincial Key Lab of Cardiovascular Research, Second Affiliated Hospital, Zhejiang University School of Medicine
- Tian Liang
- Department of Cardiology, Provincial Key Lab of Cardiovascular Research, Second Affiliated Hospital, Zhejiang University School of Medicine
- Yao Wei Lu
- Department of Cardiology, Boston Children’s Hospital, Harvard Medical School
- Xuyang Fu
- Department of Cardiology, Provincial Key Lab of Cardiovascular Research, Second Affiliated Hospital, Zhejiang University School of Medicine
- Xiaoxuan Dong
- Department of Cardiology, Provincial Key Lab of Cardiovascular Research, Second Affiliated Hospital, Zhejiang University School of Medicine
- Linbin Pu
- Department of Cardiology, Provincial Key Lab of Cardiovascular Research, Second Affiliated Hospital, Zhejiang University School of Medicine
- Tingting Hong
- Department of Cardiology, Provincial Key Lab of Cardiovascular Research, Second Affiliated Hospital, Zhejiang University School of Medicine
- Yuxia Zhou
- Institute of Translational Medicine, Zhejiang University School of Medicine
- Yu Zhang
- Department of Clinical Pharmacy, the First Affiliated Hospital, Zhejiang University School of Medicine
- Ning Liu
- Department of Cardiology, Provincial Key Lab of Cardiovascular Research, Second Affiliated Hospital, Zhejiang University School of Medicine
- Feng Zhang
- Department of Cardiology, Provincial Key Lab of Cardiovascular Research, Second Affiliated Hospital, Zhejiang University School of Medicine
- Jianming Liu
- Department of Cardiology, Boston Children’s Hospital, Harvard Medical School
- Andrea P. Malizia
- Department of Cardiology, Boston Children’s Hospital, Harvard Medical School
- Hong Yu
- Department of Cardiology, Provincial Key Lab of Cardiovascular Research, Second Affiliated Hospital, Zhejiang University School of Medicine
- Wei Zhu
- Department of Cardiology, Provincial Key Lab of Cardiovascular Research, Second Affiliated Hospital, Zhejiang University School of Medicine
- Douglas B. Cowan
- Vascular Biology Program, Boston Children’s Hospital, Harvard Medical School
- Hong Chen
- Vascular Biology Program, Boston Children’s Hospital, Harvard Medical School
- Xinyang Hu
- Department of Cardiology, Provincial Key Lab of Cardiovascular Research, Second Affiliated Hospital, Zhejiang University School of Medicine
- John D. Mably
- Center for Regenerative Medicine, University of South Florida Health Heart Institute, Morsani School of Medicine, University of South Florida
- Jian’an Wang
- Department of Cardiology, Provincial Key Lab of Cardiovascular Research, Second Affiliated Hospital, Zhejiang University School of Medicine
- Da-Zhi Wang
- Department of Cardiology, Boston Children’s Hospital, Harvard Medical School
- Jinghai Chen
- Department of Cardiology, Provincial Key Lab of Cardiovascular Research, Second Affiliated Hospital, Zhejiang University School of Medicine
- DOI
- https://doi.org/10.1038/s41467-023-37291-5
- Journal volume & issue
-
Vol. 14,
no. 1
pp. 1 – 20
Abstract
The heart requires high levels of mitochondria to sustain function, and mitochondrial stressors can be transmitted to the nucleus and reprogram metabolism. Here, the authors show that a mitochondrial ribosomal protein is important for heart development in mice by increasing nuclear Klf15 expression.
