The Role of the cGAS/STING Pathway in Arsenic-Induced Neurotoxicity: Insights from the Crosstalk Between Astrocytes and Neurons.

Arsenic is a detrimental environmental toxicant linked to neurological damage; however, the mechanisms involved remain incompletely understood. Chronic proinflammatory responses are thought to play a central role in arsenic-induced neurotoxicity. Astrocytes, which are the predominant glial cells in the central nervous system (CNS), release significant amounts of proinflammatory cytokines upon overactivation.

Neurotransmitter Metabolism in Arsenic Exposure-Induced Cognitive Impairment: Emerging Insights and Predictive Implications.

Scholars have long been interested in the association between arsenic (As) exposure and neurological disorders; however, existing systematic epidemiological investigations are insufficient and lack the inclusion of diagnostic or predictive biological markers. This study sought to evaluate the association between As exposure and cognitive impairment and identify potential biomarkers by developing predictive models. Here, we found that logarithm (Ln)-transformed urinary As concentrations were negatively linearly related to the mini-mental state examination (MMSE) score exposure-response curves.

C/EBPβ-TFAM-Mediated NLRP3 Inflammasome Activation Contributes to Arsenic-Induced Rat Kidney Injury.

Compelling evidence has demonstrated that arsenic (As) exposure is associated with kidney injuries. Given that inflammatory responses and immune imbalances are the root causes of several kidney diseases, this study investigated the potential mechanisms underlying NLRP3 inflammasome activation in As-induced kidney injury. A rat model of sub-chronic As exposure was established via oral administration of NaAsO.

Transformer 2 alpha homolog is a downstream gene of hypoxia-inducible factor 1 subunit alpha and is involved in the progression of pancreatic cancer.

Intratumoral hypoxia is a common feature of pancreatic cancer (PC) and also plays a role in its progression. However, hypoxia-regulated signatures in PC are still not completely understood. This study aimed to identify core hypoxia-associated genes and determine their underlying molecular mechanisms in PC cells.