ArticleThe Journal of cell biology2019
Respiratory chain inactivation links cartilage-mediated growth retardation to mitochondrial diseases.
Article in The Journal of cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- Vertebral BMSC-EVs under estrogen deficiency drive senescence-related mitochondrial dysfunction in endplate chondrocytes via MRPL1 mRNA delivery.Experimental & molecular medicine · 2026Article
- First Latin American Case of MLASA2 Caused by a Pathogenic Variant in the Anticodon-Binding Domain ofInternational journal of molecular sciences · 2025Article
- Metabolic rewiring caused by mitochondrial dysfunction promotes mTORC1-dependent skeletal aging.Science advances · 2025Article
- The pentose phosphate pathway controls oxidative protein folding and prevents ferroptosis in chondrocytes.Nature metabolism · 2025Article
- HIF1 activation safeguards cortical bone formation against impaired oxidative phosphorylation.JCI insight · 2024Article
- The Emerging Role of the Mitochondrial Respiratory Chain in Skeletal Aging.Aging and disease · 2024Review
- Reprogramming of Mitochondrial Respiratory Chain Complex by Targeting SIRT3-COX4I2 Axis Attenuates Osteoarthritis Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Phenotypic spectrum and clinical course of single large-scale mitochondrial DNA deletion disease in the paediatric population: a multicentre study.Journal of medical genetics · 2023Article
- EMILIN1 deficiency causes arterial tortuosity with osteopenia and connects impaired elastogenesis with defective collagen fibrillogenesis.American journal of human genetics · 2022Article
- A critical bioenergetic switch is regulated by IGF2 during murine cartilage development.Communications biology · 2022Article
- The Metabolic Landscape in Osteoarthritis.Aging and disease · 2022Article
- Ablation of the miRNA cluster 24 in cartilage and osteoblasts impairs bone remodeling.Scientific reports · 2022Article
- HIF-1α in Osteoarthritis: From Pathogenesis to Therapeutic Implications.Frontiers in pharmacology · 2022Review
- An atlas of mitochondrial DNA genotype-phenotype associations in the UK Biobank.Nature genetics · 2021Article
- Glycogen synthase kinase 3 alpha/beta deletion induces precocious growth plate remodeling in mice.Journal of molecular medicine (Berlin, Germany) · 2021Article
- Camptocormia and Other Orthopedic Compromise Dominating Mitochondrial Disorder: A Case Report.Cureus · 2020Article
- Review
- An altered heparan sulfate structure in the articular cartilage protects against osteoarthritis.Osteoarthritis and cartilage · 2020Article
- Prematurely aging mitochondrial DNA mutator mice display subchondral osteopenia and chondrocyte hypertrophy without further osteoarthritis features.Scientific reports · 2020Article
- RGS12 is required for the maintenance of mitochondrial function during skeletal development.Cell discovery · 2020Article
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In childhood, skeletal growth is driven by transient expansion of cartilage in the growth plate. The common belief is that energy production in this hypoxic tissue mainly relies on anaerobic glycolysis and not on mitochondrial respiratory chain (RC) activity. However, children with mitochondrial diseases causing RC dysfunction often present with short stature, which indicates that RC activity may be essential for cartilage-mediated skeletal growth. To elucidate the role of the mitochondrial RC in cartilage growth and pathology, we generated mice with impaired RC function in cartilage. These mice develop normally until birth, but their later growth is retarded. A detailed molecular analysis revealed that metabolic signaling and extracellular matrix formation is disturbed and induces cell death at the cartilage-bone junction to cause a chondrodysplasia-like phenotype. Hence, the results demonstrate the overall importance of the metabolic switch from fetal glycolysis to postnatal RC activation in growth plate cartilage and explain why RC dysfunction can cause short stature in children with mitochondrial diseases.
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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.