Literature DB >> 25511702

Transmitochondrial mito-miceΔ and mtDNA mutator mice, but not aged mice, share the same spectrum of musculoskeletal disorders.

Takayuki Mito1, Hikari Ishizaki1, Michiko Suzuki1, Hitomi Morishima1, Azusa Ota1, Kaori Ishikawa1, Kazuto Nakada2, Akiteru Maeno3, Toshihiko Shiroishi3, Jun-Ichi Hayashi4.   

Abstract

The spectra of phenotypes associated with aging and mitochondrial diseases sometimes appear to overlap with each other. We used aged mice and a mouse model of mitochondrial diseases (transmitochondrial mito-miceΔ with deleted mtDNA) to study whether premature aging phenotypes observed in mtDNA mutator mice are associated with aging or mitochondrial diseases. Here, we provide convincing evidence that all the mice examined had musculoskeletal disorders of osteoporosis and muscle atrophy, which correspond to phenotypes prevalently observed in the elderly. However, precise investigation of musculoskeletal disorders revealed that the spectra of osteoporosis and muscle atrophy phenotypes in mtDNA mutator mice were very close to those in mito-miceΔ, but different from those of aged mice. Therefore, mtDNA mutator mice and mito-miceΔ, but not aged mice, share the spectra of musculoskeletal disorders.
Copyright © 2014 Elsevier Inc. All rights reserved.

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Keywords:  Aging; Mito-miceΔ; Mitochondrial diseases; Osteoporosis; Sarcopenia; mtDNA mutator mice

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Year:  2014        PMID: 25511702     DOI: 10.1016/j.bbrc.2014.12.009

Source DB:  PubMed          Journal:  Biochem Biophys Res Commun        ISSN: 0006-291X            Impact factor:   3.575


  1 in total

1.  Mito-mice∆ and mitochondrial DNA mutator mice as models of human osteoporosis caused not by aging but by hyperparathyroidism.

Authors:  Takayuki Mito; Haruna Tani; Michiko Suzuki; Kaori Ishikawa; Kazuto Nakada; Jun-Ichi Hayashi
Journal:  Exp Anim       Date:  2018-07-04
  1 in total

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