ArticleNature communications2022
Impaired mitochondrial oxidative metabolism in skeletal progenitor cells leads to musculoskeletal disintegration.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
28 citing papers in PubMed, 34 citations in OpenAlex.
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- Temporal-responsive hydrogels reprogramming energy metabolic pathway in the bone-angiogenic cascade for diabetic bone regeneration.Materials today. Bio · 2026Article
- Adipose-derived CLEC3B promotes osteogenesis through a CLEC3B-IGFBP4-related paracrine axis associated with mitochondrial adaptation in postmenopausal osteoporosis.Cell biology and toxicology · 2026Article
- Mitochondria-related gene and protein changes in craniosynostosis: integrated transcriptomics and Fgfr2C361Y/+ cranial suture proteomics.Functional & integrative genomics · 2026Article
- USP24-dependent STAT2 stabilization mediates physiologic and pathologic bone formation.Cell death & disease · 2026Article
- Bioinspired, Mitochondria-Targeted Single-Atom Nanozyme Enhances Bone Regeneration by Reprogramming Stem Cell Energy Metabolism.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- Mcu regulates bone formation via mitochondrial calcium uptake and lineage allocation.Experimental & molecular medicine · 2026Article
- Exosome-mediated Piezo1 activation in 3D-printed titanium scaffolds promotes repair of femoral head osteonecrosis.Journal of nanobiotechnology · 2026Article
- Histone arginine demethylase JMJD7 promotes bone formation through regulating α-Ketoglutarate metabolism.Cell death and differentiation · 2026Article
- Review
- Bioengineered apoptotic vesicles overcome energy crisis in bone regeneration through mitochondrial metabolic activation.Bioactive materials · 2026Article
- Unraveling the genomic architecture of hock conformation defects in Pura Raza Española horses.Journal of animal science · 2026Article
- Anoctamin 5 mutation leads to abnormal bone homeostasis of GDD by regulating AMPK-dependent glucose metabolism.Frontiers in endocrinology · 2026Article
- A Study of Skeletal Stem Cell Dynamics and Its Potential Applications in the Design of a Titanium Implant for Senile Osteoporosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Organelle-tuning condition robustly fabricates energetic mitochondria for cartilage regeneration.Bone research · 2025Article
- Establishment of human periodontal ligament cell lines withFrontiers in cell and developmental biology · 2025Article
- Ultrasound-triggered piezoelectric polyetheretherketone with boosted osteogenesis via regulating Akt/GSK3β/β-catenin pathway.Journal of nanobiotechnology · 2024Article
- Bone metabolism - an underappreciated player.npj metabolic health and disease · 2024Review
- Metabolic regulation of skeletal cell fate and function.Nature reviews. Endocrinology · 2024Review
- Mitochondrial heterogeneity and adaptations to cellular needs.Nature cell biology · 2024Review
Corrections and comments
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Authors and funding
20 authors at 5 institutions in 1 country.
Funding
Abstract
Although skeletal progenitors provide a reservoir for bone-forming osteoblasts, the major energy source for their osteogenesis remains unclear. Here, we demonstrate a requirement for mitochondrial oxidative phosphorylation in the osteogenic commitment and differentiation of skeletal progenitors. Deletion of Evolutionarily Conserved Signaling Intermediate in Toll pathways (ECSIT) in skeletal progenitors hinders bone formation and regeneration, resulting in skeletal deformity, defects in the bone marrow niche and spontaneous fractures followed by persistent nonunion. Upon skeletal fracture, Ecsit-deficient skeletal progenitors migrate to adjacent skeletal muscle causing muscle atrophy. These phenotypes are intrinsic to ECSIT function in skeletal progenitors, as little skeletal abnormalities were observed in mice lacking Ecsit in committed osteoprogenitors or mature osteoblasts. Mechanistically, Ecsit deletion in skeletal progenitors impairs mitochondrial complex assembly and mitochondrial oxidative phosphorylation and elevates glycolysis. ECSIT-associated skeletal phenotypes were reversed by in vivo reconstitution with wild-type ECSIT expression, but not a mutant displaying defective mitochondrial localization. Collectively, these findings identify mitochondrial oxidative phosphorylation as the prominent energy-driving force for osteogenesis of skeletal progenitors, governing musculoskeletal integrity.
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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 OpenQuestion graph.