Di (2-ethylhexyl) phthalate and polystyrene microplastics co-exposure caused oxidative stress to activate NF-κB/NLRP3 pathway aggravated pyroptosis and inflammation in mouse kidney.

Polystyrene microplastic (PS-MPs) contamination has become a worldwide hotspot of concern, and its entry into organisms can cause oxidative stress resulting in multi-organ damage. The plasticizer di (2-ethylhexyl) phthalate (DEHP) is a common endocrine disruptor, these two environmental toxins often occur together, but their combined toxicity to the kidney and its mechanism of toxicity are unknown. Therefore, in this study, we established PS-MPS and/or DEHP-exposed mouse models.

MiR-129-3p regulates ferroptosis in the liver of Selenium-deficient broilers by targeting SLC7A11.

Selenium (Se) has been proven to be an essential trace element for organism. Se deficiency in poultry can cause widespread damage, such as exudative diathesis. The liver is not only the main organ of metabolism, but also one of the organs with high Se content in organism.

MiR-1656 targets GPX4 to trigger pyroptosis in broilers kidney tissues by activating NLRP3 inflammasome under Se deficiency.

Selenium (Se) is a vital minor element for the organism. Se deficiency caused inflammation in kidney tissue and regulate the expression of selenoproteins and microRNAs (miRNAs). Pyroptosis involved in the inflammatory response, however, whether microRNA targets GPX4 to regulate Se-deficient kidney tissue pyroptosis is unclear.

MiR-144-3p targets STC1 to activate PI3K/AKT pathway to induce cell apoptosis and cell cycle arrest in selenium deficiency broilers.

Selenium (Se) is an indispensable trace element in vertebrate. Se deficiency can damage the immune system. Studies have shown that Se deficiency can cause immune organ damage by regulating the expression of microRNA.