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Mitochondrial Genetics and Function as Determinants of Bone Phenotype and Aging

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Abstract

Purpose of Review

The purpose of this review is to summarize the recently published scientific literature regarding the effects of mitochondrial function and mitochondrial genome mutations on bone phenotype and aging.

Recent Findings

While aging and sex steroid levels have traditionally been considered the most important risk factors for development of osteoporosis, mitochondrial function and genetics are being increasingly recognized as important determinants of bone health. Recent studies indicate that mitochondrial genome variants found in different human populations determine the risk of complex degenerative diseases. We propose that osteoporosis should be among such diseases. Studies have shown the deleterious effects of mitochondrial DNA mutations and mitochondrial dysfunction on bone homeostasis. Mediators of such effects include oxidative stress, mitochondrial permeability transition, and dysregulation of autophagy.

Summary

Mitochondrial health plays an important role in bone homeostasis and aging, and understanding underlying mechanisms is critical in leveraging this relationship clinically for therapeutic benefit.

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Papers of particular interest, published recently, have been highlighted as: • Of importance •• Of major importance

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Funding

R. A. E. is supported by NIH grants R01 AR072601, R01 AG076786, and R21 AR080291.

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Authors and Affiliations

  1. Center for Musculoskeletal Research, University of Rochester School of Medicine and Dentistry, Rochester, USA

    Sarah E. Catheline & Roman A. Eliseev

  2. Department of Pharmacology and Physiology, University of Rochester School of Medicine and Dentistry, Rochester, USA

    Ethan Kaiser & Roman A. Eliseev

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  1. Sarah E. Catheline
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Correspondence to Roman A. Eliseev.

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Catheline, S.E., Kaiser, E. & Eliseev, R.A. Mitochondrial Genetics and Function as Determinants of Bone Phenotype and Aging. Curr Osteoporos Rep 21, 540–551 (2023). https://doi.org/10.1007/s11914-023-00816-4

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  • DOI: https://doi.org/10.1007/s11914-023-00816-4

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