| First Author | Ding Y | Year | 2023 |
| Journal | Cell Death Dis | Volume | 14 |
| Issue | 6 | Pages | 376 |
| PubMed ID | 37365185 | Mgi Jnum | J:337432 |
| Mgi Id | MGI:7494586 | Doi | 10.1038/s41419-023-05904-y |
| Citation | Ding Y, et al. (2023) Myeloid-derived growth factor alleviates non-alcoholic fatty liver disease alleviates in a manner involving IKKbeta/NF-kappaB signaling. Cell Death Dis 14(6):376 |
| abstractText | Whether bone marrow modulates systemic metabolism remains unknown. Our recent study suggested that myeloid-derived growth factor (MYDGF) improves insulin resistance. Here, we found that myeloid cell-specific MYDGF deficiency aggravated hepatic inflammation, lipogenesis, and steatosis, and show that myeloid cell-derived MYDGF restoration alleviated hepatic inflammation, lipogenesis, and steatosis. Additionally, recombinant MYDGF attenuated inflammation, lipogenesis, and fat deposition in primary mouse hepatocytes (PMHs). Importantly, inhibitor kappa B kinase beta/nuclear factor-kappa B (IKKbeta/NF-kappaB) signaling is involved in protection of MYDGF on non-alcoholic fatty liver disease (NAFLD). These data revealed that myeloid cell-derived MYDGF alleviates NAFLD and inflammation in a manner involving IKKbeta/NF-kappaB signaling, and serves as a factor involved in the crosstalk between the liver and bone marrow that regulates liver fat metabolism. Bone marrow functions as an endocrine organ and serves as a potential therapeutic target for metabolic disorders. |
