Autophagy Suppresses CCL2 to Preserve Appetite and Prevent Lethal Cachexia.

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Tác giả: Johan Abram-Saliba, Tracy G Anthony, Aditya Dharani, Steven M Dunn, Maria Gomez-Jenkins, Marcus D Goncalves, Zhixian Hu, Maria Ibrahim, Tobias Janowitz, Edmund C Lattime, Eduardo Cararo Lopes, Emily T Mirek, Yuri Pritykin, Joshua D Rabinowitz, Akshada Sawant, Adina Scheinfeld, Sarah Siddiqui, Xiaoyang Su, Michael Sun, Eileen White, Zhengqiao Zhao

Ngôn ngữ: eng

Ký hiệu phân loại: 785.13 *Trios

Thông tin xuất bản: United States : bioRxiv : the preprint server for biology , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 682679

UNLABELLED: Macroautophagy (autophagy hereafter) captures intracellular components and delivers them to lysosomes for degradation and recycling KEY POINTS OF PAPER: 1) Autophagy-deficient mice have reduced food intake, systemic inflammation, and cachexia2) CCL2, but not GDF15 or CXCL10, induces lethal cachexia caused by autophagy defect3) Autophagy-deficient mice have CCL2-dependent destruction of appetite-promoting neurons in the hypothalamus4) Leptin deficiency restores appetite and rescues lethal cachexia in autophagy-deficient mice5) Autophagy-deficient mice die from cachexia mediated by appetite loss6) Degenerative conditions due to impaired autophagy are caused by the inflammatory response to the damage7) Targeting CCL2 may be a viable approach to prevent degenerative wasting disorders.
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