ArticlePLoS biology2024
Adenosine diphosphate released from stressed cells triggers mitochondrial transfer to achieve tissue homeostasis.
Article in PLoS biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Cellular Mechanisms Enabling Mitochondria Transfer and Transplantation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Purinergic signaling in osteoarthritis: Mechanistic insights into pathogenesis and therapeutic targeting.Genes & diseases · 2026Review
- Bone organoids and mitochondrial reprogramming.Journal of orthopaedic translation · 2026Review
- Therapeutic effect of mitochondrial transfer on bone tissue diseases: treatment strategy of mitochondrial transplantation and delivery technology.Journal of orthopaedic translation · 2026Review
- Mitochondrial Transport in Bone Metabolism Homeostasis: Molecular Mechanisms and Targeted Therapeutic Strategies.International journal of molecular sciences · 2026Review
- Mitochondrial DNA mutations and intercellular mitochondrial transfer in cancer: mechanisms, biological effects, and clinical potential.Biomarker research · 2026Review
- Mitochondrial Dysfunction in Cardiac Diseases: Insights into Pathophysiology and Clinical Outcomes.Current cardiology reviews · 2026Review
- Regulation of Mitochondrial Homeostasis: Applications of Nanobiomaterials in Age-Related Bone Diseases.International journal of nanomedicine · 2026Review
- The hidden driver of osteoporosis: mitochondria-dominated inflammation.Cell communication and signaling : CCS · 2025Review
- Mesenchymal stromal cell-mediated mitochondrial transfer unveils new frontiers in disease therapy.Stem cell research & therapy · 2025Review
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17 authors.
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Abstract
Cell-to-cell mitochondrial transfer has recently been shown to play a role in maintaining physiological functions of cell. We previously illustrated that mitochondrial transfer within osteocyte dendritic network regulates bone tissue homeostasis. However, the mechanism of triggering this process has not been explored. Here, we showed that stressed osteocytes in mice release adenosine diphosphate (ADP), resulting in triggering mitochondrial transfer from healthy osteocytes to restore the oxygen consumption rate (OCR) and to alleviate reactive oxygen species accumulation. Furthermore, we identified that P2Y2 and P2Y6 transduced the ADP signal to regulate osteocyte mitochondrial transfer. We showed that mitochondrial metabolism is impaired in aged osteocytes, and there were more extracellular nucleotides release into the matrix in aged cortical bone due to compromised membrane integrity. Conditioned medium from aged osteocytes triggered mitochondrial transfer between osteocytes to enhance the energy metabolism. Together, using osteocyte as an example, this study showed new insights into how extracellular ADP triggers healthy cells to rescue energy metabolism crisis in stressed cells via mitochondrial transfer in tissue homeostasis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.