J
James L. Kirkland
Researcher at Mayo Clinic
Publications - 322
Citations - 33834
James L. Kirkland is an academic researcher from Mayo Clinic. The author has contributed to research in topics: Senescence & Adipose tissue. The author has an hindex of 76, co-authored 280 publications receiving 23328 citations. Previous affiliations of James L. Kirkland include Buck Institute for Research on Aging & University of Pittsburgh.
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Journal ArticleDOI
The biochemistry of mammalian senescence
TL;DR: The fundamental cause of senescence remains elusive but might, as in the case of other biological processes which are phylogenetically widespread, turn out to be quite simple, and perhaps, even modifiable.
Book ChapterDOI
Current Views of the Fat Cell as an Endocrine Cell: Lipotoxicity
TL;DR: The causes, mechanisms, and consequences oflipotoxicity are considered, with particular regard to the role of adipose tissue in lipotoxicity in other tissues and to possible reasons why adipose tissues is resistant to lipot toxicity.
Journal ArticleDOI
Transplanted senescent renal scattered tubular-like cells induce injury in the mouse kidney.
Seo Rin Kim,Seo Rin Kim,Kai Jiang,Christopher M. Ferguson,Hui Tang,Xiao Jun Chen,Xiao Jun Chen,Xiangyang Zhu,La Tonya J. Hickson,Tamara Tchkonia,James L. Kirkland,Lilach O. Lerman +11 more
TL;DR: Exogenously delivered senescent renal STC directly injure healthy mouse kidneys and indicates the role of endogenous cellular senescence in the pathogenesis of kidney injury, and the utility of senolytic therapy is evaluated.
Journal ArticleDOI
The murine dialysis fistula model exhibits a senescence phenotype: Pathobiological mechanisms and therapeutic potential
Karl A. Nath,Daniel R. O'Brien,Anthony J. Croatt,Joseph P. Grande,Allan W. Ackerman,Meryl C. Nath,Satsuki Yamada,Andre Terzic,Tamara Tchkonia,James L. Kirkland,Zvonimir S. Katusic +10 more
TL;DR: A novel concept underlying the basis for maturational and functional failure in human dialysis AVFs is introduced and a new target for senolytic therapy is identified.
Journal ArticleDOI
Partial inhibition of mitochondrial complex I ameliorates Alzheimer’s disease pathology and cognition in APP/PS1 female mice
Andrea Stojakovic,Sergey Trushin,Anthony Sheu,Layla Khalili,Su-Youne Chang,Xing Li,Trace A. Christensen,Jeffrey L. Salisbury,Rachel E. Geroux,Benjamin Gateno,Padraig J. Flannery,Mrunal Dehankar,Cory C. Funk,Jordan Wilkins,Anna Stepanova,Tara O’Hagan,Alexander Galkin,Jarred J. Nesbitt,Xiujuan Zhu,Utkarsh Tripathi,Slobodan Macura,Tamar Tchkonia,Tamar Pirtskhalava,James L. Kirkland,Rachel A. Kudgus,Renee A. Schoon,Joel M. Reid,Yu Yamazaki,Takahisa Kanekiyo,Song Zhang,Emirhan Nemutlu,Petras P. Dzeja,Adam Jaspersen,Ye In Christopher Kwon,Michael K. Lee,Eugenia Trushina +35 more
TL;DR: The authors showed that partial inhibition of complex I triggers the AMP-activated protein kinase-dependent signaling network leading to neuroprotection in symptomatic APP/PS1 female mice, a translational model of AD.