Chia-Ling Wu
Boston University
16 Papers
36 Citations
Chia-Ling Wu is an academic researcher from Boston University. The author has contributed to research in topics: Skeletal muscle & Muscle atrophy. The author has an hindex of 12, co-authored 16 publications.
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Papers
Clonal hematopoiesis associated with Tet2 deficiency accelerates atherosclerosis development in mice
José J. Fuster,Susan MacLauchlan,María A. Zuriaga,Maya N. Polackal,Allison C. Ostriker,Raja Chakraborty,Chia-Ling Wu,Soichi Sano,Sujatha Muralidharan,Cristina Rius,Jacqueline T Vuong,Sophia Jacob,Varsha Muralidhar,Avril A. B. Robertson,Mark E. Cooper,Vicente Andrés,Karen K. Hirschi,Kathleen A. Martin,Kenneth Walsh +18 more
TL;DR: The effects of the expansion of Tet2-mutant cells in atherosclerosis-prone, low-density lipoprotein receptor–deficient mice are studied and it is found that partial bone marrow reconstitution with TET2-deficient cells was sufficient for their clonal expansion and led to a marked increase in Atherosclerotic plaque size.
Genome-wide identification of FoxO-dependent gene networks in skeletal muscle during C26 cancer cachexia
Sarah M. Judge,Chia-Ling Wu,Adam W. Beharry,Brandon M. Roberts,Leonardo F. Ferreira,Susan C. Kandarian,Andrew Judge +6 more
TL;DR: Blocking FoxO prevented C26-induced muscle fiber atrophy of both locomotor muscles and the diaphragm and significantly spared force deficits, providing new evidence that FoxO-dependent transcription is a central node controlling diverse gene networks in skeletal muscle during cancer cachexia.
Identification of Genes that Elicit Disuse Muscle Atrophy via the Transcription Factors p50 and Bcl-3
TL;DR: This work represents the first study to use a global approach to identify genes required to produce the atrophied phenotype with disuse using gene expression profiling in wild type compared to Nfkb1 (gene encodes p50) and Bcl-3 deficient mice.
Nuclear factor‐κB signalling and transcriptional regulation in skeletal muscle atrophy
TL;DR: The nuclear factor-κB signalling pathway is a necessary component of adult skeletal muscle atrophy resulting from systemic illnesses or disuse, and it is associated with activation of NF-κb transcriptional activity.
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Acute and Chronic Increases of Circulating FSTL1 Normalize Energy Substrate Metabolism in Pacing-Induced Heart Failure
Mitsuru Seki,Jeffery C. Powers,Sonomi Maruyama,María A. Zuriaga,Chia-Ling Wu,Clara Kurishima,Lydia Kim,Jesse Johnson,Anthony Poidomani,Tao Wang,Eric R. Muñoz,Sudarsan Rajan,Joon Y. Park,Kenneth Walsh,Fabio A. Recchia +14 more
TL;DR: Findings support a novel function for FSTL1 and provide the first direct evidence that a circulating cardiokine/myokine can alter myocardial and systemic energy substrate metabolism, in vivo.
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