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2016 Fiscal Year Final Research Report

Molecular mechanism of autophagic abnormality in mouse model with rhabdomyolysis

Research Project

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Project/Area Number 15K15344
Research Category

Grant-in-Aid for Challenging Exploratory Research

Allocation TypeMulti-year Fund
Research Field Metabolomics
Research InstitutionUniversity of Tsukuba

Principal Investigator

SHIMANO Hitoshi  筑波大学, 医学医療系, 教授 (20251241)

Project Period (FY) 2015-04-01 – 2017-03-31
Keywordsスタチン / 横紋筋融解症 / オートファジー / コレステロール
Outline of Final Research Achievements

This study was aimed to elucidate the mechanism of the onset of rhabdomyolysis, which is a side effect of statin which is a treatment for hypercholesterolemia. We generated skeletal muscle specific-HMGCR, a target of statin, knockout mice. The turnover between cell death and regeneration were frequently occurred in muscle cells of mKO mice, indicating that the deficiency of HMGCR in skeletal muscle leads to myopathy. We examined the relationship between myopathy and autophagy in skeletal muscle of these mice. The function of Rab7, which is involved in the formation of autolysosomes, was impaired and the degradation of autolysosomes was he also impaired in skeletal muscle of these mice. Thus, we found that the skeletal muscle cells of mKO mice exhibited the abnormality of autolysosomes and the increase of p62 protein, due to the functional abnormality of lysosome.

Free Research Field

代謝学

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Published: 2018-03-22  

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