Cell · 2025
Vagal blockade of the brain-liver axis deters cancer-associated cachexia.
СтатьяНазвание и аннотация: Перевод в очереди
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Garrett Aliesha, Darzi Naama, Deshmukh Ashlesha, Rosenfeld Nataly, Goldman Omer, Adler Lital, Bab-Dinitz Elizabeta, Singer Oded, Hassani Najafabadi Alireza, Wong Chi Wut, Bose Shree, Randon Peggy M, Bustamante Francisco, Larios Rene, Brandis Alexander, Mehlman Tevie, Smaglo Brandon, Chang Ping, Oliva Jacqueline, Haymaker Cara, Nagawekar Laukik, Wu Sophie R, Huang Yixuan, Shen Aidan, Vora Ahana, Padilla Jon Floyd, Pfeffer Alissa, Sutherland Gary, Starr Mark, Zimmers Teresa, Zhu Yangzhi, Morizio James, Erez Ayelet, Shen Xiling
Аннотация
Cancer-associated cachexia (CAC) is a multifactorial and currently incurable syndrome responsible for nearly one-third of cancer-related deaths. It contributes to therapy resistance and increases mortality among affected patients. In this study, we show that cancer-induced systemic inflammation alters vagal tone in CAC mouse models. This vagal dysregulation disrupts the brain-liver vagal axis, leading to a reprogramming of hepatic protein metabolism through the depletion of HNF4α, a key transcriptional regulator of liver function. The loss of HNF4α disrupts hepatic metabolism and promotes systemic inflammation, resulting in cachectic phenotypes. Interventions targeting the right cervical vagus nerve surgically, chemically, electrically, or through a non-invasive transcutaneous device attenuate CAC progression, alleviate its clinical manifestations, and synergize with chemotherapy to improve overall health and survival in mice.