Mitochondrial Transfer Regulates Cell Fate Through Metabolic Remodeling in Osteoporosis
Abstract: Mitochondria are the powerhouse of eukaryotic cells, which regulate cell metabolism and differentiation. Recently, mitochondrial transfer between cells has been shown to direct recipient cell fate. However, it is unclear whether mitochondria can translocate to stem cells and whether this transfer alters stem cell fate. Here, mesenchymal stem cell (MSC) regulation is examined by macrophages in the bone marrow environment. It is found that macrophages promote osteogenic differentiation of MSCs by delivering mitochondria to MSCs. However, under osteoporotic conditions, macrophages with altered phenotypes, and metabolic statuses release oxidatively damaged mitochondria. Increased mitochondrial transfer of M1‐like macrophages to MSCs triggers a reactive oxygen species burst, which leads to metabolic remodeling. It is showed that abnormal metabolism in MSCs is caused by the abnormal succinate accumulation, which is a key factor in abnormal osteogenic differentiation. These results reveal that mitochondrial transfer from macrophages to MSCs allows metabolic crosstalk to regulate bone homeostasis. This mechanism identifies a potential target for the treatment of osteoporosis.
- Location
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Deutsche Nationalbibliothek Frankfurt am Main
- Extent
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Online-Ressource
- Language
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Englisch
- Bibliographic citation
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Mitochondrial Transfer Regulates Cell Fate Through Metabolic Remodeling in Osteoporosis ; day:11 ; month:12 ; year:2022 ; extent:15
Advanced science ; (11.12.2022) (gesamt 15)
- Creator
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Cai, Wenjin
Zhang, Jinglun
Yu, Yiqian
Ni, Yueqi
Wei, Yan
Cheng, Yihong
Han, Litian
Xiao, Leyi
Ma, Xiaoxin
Wei, Hongjiang
Ji, Yaoting
Zhang, Yufeng
- DOI
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10.1002/advs.202204871
- URN
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urn:nbn:de:101:1-2022121214110665919859
- Rights
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Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
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15.08.2025, 7:26 AM CEST
Data provider
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Associated
- Cai, Wenjin
- Zhang, Jinglun
- Yu, Yiqian
- Ni, Yueqi
- Wei, Yan
- Cheng, Yihong
- Han, Litian
- Xiao, Leyi
- Ma, Xiaoxin
- Wei, Hongjiang
- Ji, Yaoting
- Zhang, Yufeng
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Mettl3-mediated m6A RNA methylation regulates the fate of bone marrow mesenchymal stem cells and osteoporosis
The balance of two opposing factors Mad and Myc regulates cell fate during tissue remodeling
Differential binding of mitochondrial transcripts by MRB8170 and MRB4160 regulates distinct editing fates of mitochondrial mRNA in trypanosomes
Chromatin remodeling in tissue stem cell fate determination
Lipocalin 2 regulates mitochondrial phospholipidome remodeling, dynamics, and function in brown adipose tissue in male mice
Mitochondrial matrix-localized Src kinase regulates mitochondrial morphology
TFEB intrinsically regulates mitochondrial functions
Fate mapping RNA-sequencing reveal Malat1 regulates Sca1+ progenitor cells to vascular smooth muscle cells transition in vascular remodeling
REPIN1 regulates iron metabolism and osteoblast apoptosis in osteoporosis
JNK regulates muscle remodeling via myostatin/SMAD inhibition
NDUFS4 regulates cristae remodeling in diabetic kidney disease
Author Correction: Lipocalin 2 regulates mitochondrial phospholipidome remodeling, dynamics, and function in brown adipose tissue in male mice
Mettl3-mediated m6A RNA methylation regulates the fate of bone marrow mesenchymal stem cells and osteoporosis
The balance of two opposing factors Mad and Myc regulates cell fate during tissue remodeling
Differential binding of mitochondrial transcripts by MRB8170 and MRB4160 regulates distinct editing fates of mitochondrial mRNA in trypanosomes
Chromatin remodeling in tissue stem cell fate determination
Lipocalin 2 regulates mitochondrial phospholipidome remodeling, dynamics, and function in brown adipose tissue in male mice
Mitochondrial matrix-localized Src kinase regulates mitochondrial morphology
TFEB intrinsically regulates mitochondrial functions
Fate mapping RNA-sequencing reveal Malat1 regulates Sca1+ progenitor cells to vascular smooth muscle cells transition in vascular remodeling
REPIN1 regulates iron metabolism and osteoblast apoptosis in osteoporosis
JNK regulates muscle remodeling via myostatin/SMAD inhibition
NDUFS4 regulates cristae remodeling in diabetic kidney disease