| First Author | Wang M | Year | 2021 |
| Journal | iScience | Volume | 24 |
| Issue | 7 | Pages | 102766 |
| PubMed ID | 34286232 | Mgi Jnum | J:338667 |
| Mgi Id | MGI:6828536 | Doi | 10.1016/j.isci.2021.102766 |
| Citation | Wang M, et al. (2021) Programmed PPAR-alpha downregulation induces inflammaging by suppressing fatty acid catabolism in monocytes. iScience 24(7):102766 |
| abstractText | Inflammaging is associated with an increased risk of chronic disease. Monocytes are the principal immune cells for the production of inflammatory cytokines and contribute to inflammaging in the elderly. However, the underlying mechanisms remain largely unknown. Here, we found that monocytes from aged individuals contained high levels of lipid droplets (LDs), and this increase was correlated with impaired fatty acid oxidation. Downregulated peroxisome proliferator-activated receptor (PPAR)-alpha may be responsible for the pro-inflammatory phenotype of monocytes in aged individuals, as it was positively correlated with LD accumulation and increasing TNF-alpha concentration. Interestingly, interventions that result in PPAR-alpha upregulation, such as fenofibrate treatment, TNF-alpha neutralization, or calorie restriction, reversed the effect of aging on monocytes. Thus the downregulation of PPAR-alpha and LD levels in monocytes represents a novel biomarker for inflammaging. Furthermore, PPAR-alpha activation in the elderly may also alleviate long-term inflammaging, preventing the development of life-limiting chronic diseases. |
