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James M. Flynn

Researcher at Buck Institute for Research on Aging

Publications -  19
Citations -  1411

James M. Flynn is an academic researcher from Buck Institute for Research on Aging. The author has contributed to research in topics: Mitochondrion & Oxidative stress. The author has an hindex of 15, co-authored 19 publications receiving 1152 citations. Previous affiliations of James M. Flynn include University of North Texas Health Science Center.

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Late-life rapamycin treatment reverses age-related heart dysfunction

TL;DR: It is proposed that late‐life rapamycin therapy not only extends the lifespan of mammals, but also confers functional benefits to a number of tissues and mechanistically implicates an improvement in contractile function and antihypertrophic signaling in the aged heart with a reduction in age‐related inflammation.
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SOD2 in mitochondrial dysfunction and neurodegeneration.

TL;DR: SOD2's potential involvement in the progression of neurodegenerative diseases such as stroke and Alzheimer and Parkinson diseases, as well as its potential role in "normal" age-related cognitive decline are reviewed.
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Mitochondrial oxidative stress caused by Sod2 deficiency promotes cellular senescence and aging phenotypes in the skin

TL;DR: It is shown that the number of senescent cells, as well as impaired mitochondrial (complex II) activity increase in naturally aged mouse skin, and the idea that mitochondrial oxidative stress and cellular senescence contribute to aging skin phenotypes in vivo is supported.
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Genome-wide DNA methylation changes with age in disease-free human skeletal muscle.

TL;DR: This work reports for the first time a genome‐wide study of DNA methylation dynamics in skeletal muscle of healthy male individuals during normal human aging and identifies 500 dmCpG sites that perform well in discriminating young from old samples.