Acute Carbon Monoxide Poisoning Induces Renal Inflammation and Apoptosis

Acute carbon monoxide poisoning (ACOP), a prevalent cause of poisoning worldwide, leads to multi-organ damage, with the kidneys being particularly susceptible due to their high metabolic activity, resulting in acute kidney injury (AKI). However, the molecular mechanisms underlying CO-induced AKI remain poorly understood. It was hypothesized that ACOP induces renal injury through inflammatory and apoptotic pathways. An ACOP mouse model was developed to evaluate renal effects, with renal function assessed via serum creatinine (SCr) and blood urea nitrogen (BUN) levels. Histopathological analysis, TUNEL assay, ELISA, RNA sequencing (RNA-seq), Western blot, and qPCR were employed to investigate renal injury, inflammation, and apoptosis.