Secreted growth differentiation factor15 as a potential biomarker for mitochondrial dysfunctions in aging and age-related disorders

被引:160
作者
Fujita, Yasunori [1 ]
Taniguchi, Yu [2 ]
Shinkai, Shoji [2 ]
Tanaka, Masashi [3 ]
Ito, Masafumi [1 ]
机构
[1] Tokyo Metropolitan Inst Gerontol, Res Team Mech Aging, Tokyo, Japan
[2] Tokyo Metropolitan Inst Gerontol, Res Team Social Participat & Community Hlth, Tokyo, Japan
[3] Tokyo Metropolitan Inst Gerontol, Dept Genom Longev & Hlth, Tokyo, Japan
关键词
age-related disorders; aging; biomarker; growth differentiation factor15; mitochondrial dysfunction; MACROPHAGE INHIBITORY CYTOKINE-1; TGF-BETA SUPERFAMILY; TYPE-2; DIABETES-MELLITUS; HUMAN SKELETAL-MUSCLE; ACUTE CORONARY SYNDROME; NSAID-ACTIVATED GENE-1; FATTY-ACID OXIDATION; INSULIN-RESISTANCE; PARKINSONS-DISEASE; ALZHEIMERS-DISEASE;
D O I
10.1111/ggi.12724
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
We and other have recently shown that growth differentiation factor15 (GDF15) is a useful diagnostic marker for mitochondrial diseases, which are inherited disorders caused by mitochondrial or nuclear genomic mutations that lead to impaired energy production. As the primary cause of mitochondrial diseases is mitochondrial dysfunction, the blood level of GDF15 might reflect mitochondrial function in patients, and thus could be a marker for mitochondrial dysfunction. GDF15 has been implicated in aging and various age-related disorders, such as cardiovascular diseases and diabetes, the blood level of which is reportedly elevated in older adults as well as in patients. Although GDF15 might be induced as a result of various cellular stresses and dysfunctions, it would also be possible that the blood GDF15 level reflects at least in part mitochondrial dysfunction in aging and age-related disorders. In the present review, we summarized the current literature regarding GDF15 in aging and age-related disorders from the perspective of biomarkers, with a particular focus on mitochondrial dysfunction. Geriatr Gerontol Int 2016; 16 (Suppl. 1): 17-29.
引用
收藏
页码:17 / 29
页数:13
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