Epithelial-mesenchymal transition (EMT) refers to the conversion of epithelial cells to mesenchymal phenotype, which endows the epithelial cells with enhanced migration, invasion, and extracellular matrix production abilities. These characteristics link EMT with the pathogenesis of organ fibrosis and cancer progression. Recent studies have preliminarily established that fine particulate matter with an aerodynamic diameter of less than 2.5 μm (PM_2.5) is correlated with EMT initiation. In this pathological process, PM_2.5 particles, excessive reactive oxygen species (ROS) derived from PM_2.5, and certain components in PM_2.5, such as ions and polyaromatic hydrocarbons (PAHs), have been implicated as potential EMT mediators that are linked to the activation of transforming growth factor β (TGF-β)/SMADs, NF-κB, growth factor (GF)/extracellular signal-regulated protein kinase (ERK), GF/phosphatidylinositol 3-kinase (PI3K)/Akt, wingless/integrated (Wnt)/β-catenin, Notch, Hedgehog, high mobility group box B1 (HMGB1)-receptor for advanced glycation end-products (RAGE), and aryl hydrocarbon receptor (AHR) signaling cascades and to cytoskeleton rearrangement. These pathways directly and indirectly transduce pro-EMT signals that regulate EMT-related gene expression in epithelial cells, finally inducing the characteristic alterations in morphology and functions of epithelia. In addition, novel associations between autophagy, ATP citrate lyase (ACLY), and exosomes with PM_2.5-induced EMT have also been summarized. However, some debates and paradoxes remain to be consolidated. This review discusses the potential molecular mechanisms underlying PM_2.5-induced EMT, which might account for the latent role of PM_2.5 in cancer progression and fibrogenesis.

Background: With the development of industrialization in human society, ambient pollutants are becoming more harmful to human health. Epidemiological and toxicological studies indicate that a close relationship exists between particulate matter with a diameter ≤2.5 µm (PM_2.5) and neurodegenerative diseases such as Alzheimer's disease (AD) and Parkinson's disease (PD). To further confirm the relationship, we focus on possible relevant mechanisms of oxidative stress and neuroinflammation underlying the association between PM_2.5 and neurodegenerative diseases in the review. Methods: A literature search was performed on the studies about PM_2.5 and neurodegenerative diseases via PubMed. A total of 113 articles published were selected, and 31 studies were included. Results: PM_2.5 can enter the central nervous system through 2 main pathways, the blood–brain barrier and olfactory neurons. The inflammatory response and oxidative stress are 2 primary mechanisms via which PM_2.5 leads to toxicity in the brain. PM_2.5 abnormally activates microglia, inducing the neuroinflammatory process. Inflammatory markers such as IL-1β play an essential role in neurodegenerative diseases such as AD and PD. Moreover, the association between lipid mechanism disorders related to PM_2.5 and neurodegenerative diseases has been gaining momentum. Conclusions: In conclusion, PM_2.5 could significantly increase the risk of neurological disorders, such as AD and PD. Furthermore, any policy aimed at reducing air-polluting emissions and increasing air quality would be protective in human beings.

Low-grade inflammation (LGI) mainly acted as the mediator of the association of obesity and inflammatory diet with numerous chronic diseases, including neuropsychiatric diseases. However, the evidence about the effect of LGI on brain structure is limited but important, especially in the context of accelerating aging. This study was then designed to close the gap, and we leveraged a total of 37,699 participants from the UK Biobank and utilized inflammation score (INFLA-score) to measure LGI. We built the longitudinal relationships of INFLA-score with brain imaging phenotypes using multiple linear regression models. We further analyzed the interactive effects of specific covariates. The results showed high level inflammation reduced the volumes of the subcortex and cortex, especially the globus pallidus (β [95% confidence interval] = −0.062 [−0.083, −0.041]), thalamus (−0.053 [−0.073, −0.033]), insula (−0.052 [−0.072, −0.032]), superior temporal gyrus (−0.049 [−0.069, −0.028]), lateral orbitofrontal cortex (−0.047 [−0.068, −0.027]), and others. Most significant effects were observed among urban residents. Furthermore, males and individuals with physical frailty were susceptive to the associations. The study provided potential insights into pathological changes during disease progression and might aid in the development of preventive and control targets in an age-friendly city to promote great health and well-being for sustainable development goals.

Background: The global rise in ultra-processed food (UPF) consumption and the persistent burden of mental disorders have raised growing public health concerns. Emerging evidence suggests that unfavorable dietary patterns, particularly with high UPF intake, contribute to the development of mental disorders. Objective: To assess the associations of UPF-related metabolic signatures and mental disorders. Methods: In this population-based cohort study of 30,059 participants from the UK Biobank, we first identified a plasma metabolic signature associated with UPF intake leveraging nuclear magnetic resonance metabolomics. We then applied Cox and logistic regression models to investigate the associations of both UPF consumption and its metabolic signature with incident mental disorders and specific psychological symptoms, respectively. Results: Higher UPF intake was significantly associated with increased risks of overall mental disorder (hazard ratio per 10% increment [95% confidence interval]: 1.04 [1.02, 1.06]), depressive disorder (1.14 [1.08, 1.20]), anxiety disorder (1.12 [1.06, 1.18]), and substance use disorder (1.06 [1.01, 1.11]), as well as several psychological symptoms including suicidal ideation (odds ratios [95% confidence interval]: 1.12 [1.03, 1.16]) and anxiety feeling (1.05 [1.01, 1.09]). Similarly, the UPF-related metabolic signature was independently associated with elevated risks of these mental health outcomes and partially mediated the associations between UPF intake and mental disorders. Conclusions: These findings highlighted the potential metabolic pathways underlying the neuropsychiatric risks of UPF consumption and underscored the importance of dietary quality in mental health.