A qualitative study of barriers and facilitators to low-dose aspirin adherence in pregnancy.

Ulcerative colitis (UC) is a generic, chronic, recurrent inflammatory condition mostly affecting the mucosa and submucosa of the colorectum [, ]. The incidence and prevalence of UC have had a consistent increase in recent years []. The ailment has a prolonged duration and a diverse array of lesions []. Moreover, it is crucial to acknowledge that the primary clinical manifestations associated with this condition include recurrent diarrhea, severe abdominal pain, viscous mucus discharge, visibly blood‐stained feces, and other debilitating symptoms that significantly impair an individual′s quality of life []. Notwithstanding the availability of numerous treatments, over 15% of individuals with UC ultimately necessitate surgical intervention owing to the ineffectiveness of medicinal therapy [, ]. The expenses related to surgical complications impose a significant economic burden. The pathogenesis of UC is obscure and intricate. Evidence is increasingly indicating a close relationship between oxidative stress and inflammation, influenced by genetics, gut flora, the host immune system, and environmental variables [–]. Research examining the molecules underlying the pathophysiology of UC is crucial. In recent years, ferroptosis, a distinct form of cell death characterized by iron accumulation and lipid peroxidation, has been identified as a crucial factor in the onset and advancement of various intestinal disorders, including intestinal ischemia/reperfusion injury, inflammatory bowel disease (IBD), and colorectal cancer (CRC) [–]. Ferroptosis is governed by various cellular metabolic pathways, encompassing redox homeostasis, iron metabolism, mitochondrial function, amino acid metabolism, and lipid metabolism [, ]. An increasing number of studies have identified ferroptosis in the colonic tissues of UC patients and animal models of the condition [, , ]. The principal events of ferroptosis are intricately linked to the pathogenic mechanisms of UC, encompassing glutathione depletion, GPX4 inactivation, lipid peroxidation, iron homeostasis disruption, and lipoxygenase overexpression [, ]. Ferroptosis contributes to persistent inflammation in UC by inducing deadly reactive oxygen species (ROS) buildup, iron overload, and unregulated lipid peroxidation, leading to the demise of intestinal epithelial cells (IECs) []. Notwithstanding these findings, the significance and mechanisms of ferroptosis in UC remain ambiguous and necessitate additional investigation. Tissue inhibitor Metalloproteinase 1 (TIMP1), sometimes referred to as EPA, is a member of a metalloproteinase family that prevents the degradation of the extracellular matrix []. TIMP1 has been documented in numerous conditions, including subarachnoid hemorrhage, different malignancies, ischemic stroke, Type 2 diabetic osteoporosis, and UC [–]. In individuals with IBD, TIMP1 expression is markedly increased in colonic tissue and serum, corresponding with the severity of the disease []. Moreover, bioinformatics has recognized TIMP1 in the context of ferroptosis. In Type 2 diabetic osteoporosis, the knockdown of TIMP1 suppresses ferroptosis in osteoblasts triggered by elevated glucose and lipid levels []. Zhang et al. [] demonstrate that TIMP1 is identified as one of the four ferroptosis‐related genes (TIMP1, LPIN1, SOCS1, and CD44) possessing diagnostic significance for UC. The expression of the four genes is elevated in dextran sulfate sodium (DSS) salt–induced mice colitis and correlates with several immune cells, including neutrophils, M0 and M1 macrophages, B cells, and NK cells []. Moreover, TIMP1 is a principal target via which oxymatrine regulates ferroptosis and inflammation in UC []. The treatment of oxymatrine inhibits the expression of key genes, such as TIMP1, and mitigates the pathological damage linked to UC by enhancing ferroptosis and inflammatory responses in colonic tissue []. Although numerous studies have recognized the role of TIMP1 in the ferroptosis associated with UC, limited research has investigated the precise function of TIMP1 at the single‐gene level in this context.