| Texto completo | |
| Autor(es): |
Campolim, Clara Machado
;
Schimenes, Bianca Camilo
;
Veras, Mariana Matera
;
Kim, Young-Bum
;
Prada, Patricia Oliveira
Número total de Autores: 5
|
| Tipo de documento: | Artigo Científico |
| Fonte: | FRONTIERS IN IMMUNOLOGY; v. 15, p. 8-pg., 2024-06-12. |
| Resumo | |
Air pollution is an urgent concern linked to numerous health problems in low- and middle-income countries, where 92% of air pollution-related deaths occur. Particulate matter 2.5 (PM2.5) is the most harmful component of air pollutants, increasing inflammation and changing gut microbiota, favoring obesity, type 2 diabetes, and Alzheimer's Disease (AD). PM2.5 contains lipopolysaccharides (LPS), which can activate the Toll-like receptor 4 (TLR4) signaling pathway. This pathway can lead to the release of pro-inflammatory markers, including interleukins, and suppressor of cytokine signaling-3 (SOCS3), which inhibits leptin action, a hormone that keeps the energy homeostasis. Leptin plays a role in preventing amyloid plaque deposition and hyperphosphorylation of tau-protein (p-tau), mechanisms involved in the neurodegeneration in AD. Approximately 50 million people worldwide are affected by dementia, with a significant proportion living in low-and middle-income countries. This number is expected to triple by 2050. This mini-review focuses on the potential impact of PM2.5 exposure on the TLR4 signaling pathway, its contribution to leptin resistance, and dysbiosis that exacerbates the link between obesity and AD. (AU) | |
| Processo FAPESP: | 17/18498-6 - Impacto da exposição perinatal a poluentes ambientais na gênese da obesidade e diabetes mellitus tipo 2: aspectos metabólicos e epigenéticos |
| Beneficiário: | Patrícia de Oliveira Prada |
| Modalidade de apoio: | Auxílio à Pesquisa - Regular |