Ferroptosis is a new form of programmed cell death due to iron-dependent excess accumulation of lipid peroxides and differs from other programmed cell deaths in morphological and biochemical characteristics. The process of ferroptosis is precisely regulated by iron metabolism, lipid metabolism, amino acid metabolism, and numerous signaling pathways, and plays a complex role in many pathophysiological processes. Recent studies have found that ferroptosis is closely associated with the development and progression of many lung diseases, including acute lung injury, pulmonary ischemia-reperfusion injury, lung cancer, chronic obstructive pulmonary disease, and pulmonary fibrosis. Here, we present a review of the main regulatory mechanisms of ferroptosis and its research progress in the pathogenesis and treatment of lung diseases, with the aim of providing new ideas for basic and clinical research of lung-related diseases.
Purpose: To evaluate whether ferroptosis is involved in hyperoxic acute lung injury (HALI) and its mechanisms through the HALI model. Methods: HE staining was used to assess lung injury pathology after the establishment of neonatal rat HALI model. ELISA was used to detect ROS, GPX4, and GSH expression. Prussian blue staining and Western Blot were used to detect iron deposition and the expression of ferroptosis-related proteins, respectively. Results: The HALI group showed pathological changes with larger and fewer alveoli and thicker alveolar septa after HE staining. Prussian blue staining detected significant iron deposition in the lung tissue of the HALI group. GPX4, GSH, GSS, and SLC7A11 expressions were significantly decreased in the HALI group than in the normal control group. In contrast, ROS, TFRC, FHC, and FLC expressions showed opposite results (p<0.05).
Conclusion:Ferroptosis may be involved in the pathological process of hyperoxic lung injury in neonatal rats.
Peptidyl deiminase 4 (PADI4) catalyzes peptidylarginine to citrulline. The gene encoding PADI4 is associated with rheumatoid arthritis (RA) in some populations. The levels of PADI4, anti-CCP, and RF were measured in the blood of patients suffering from RA and osteoarthritis (OA) for less than six months using ELISA. The levels were also measured in the blood of patients that have been diagnosed with RA for more than three years. As controls, samples from healthy subjects or patients with ankylosing spondylitis (AS), epidemic pleurodynia (EP), OA, psoriatic arthritis (PA), systemic lupus erythematosus (SLE), gouty arthritis (GA), or Still’s disease (ST) were also assayed. Of patients with early RA, 68.7% had significantly higher levels of PADI4 than patients with early OA. Patients with RA for a longer period of time had a higher expression of PADI4 than patients with SLE, ST, and GA, but they were similar to healthy subjects or patients with AS, EP, OA, or PA. The level of PADI4 was significantly correlated to the levels of RF and anti-CCP in blood samples of RA, but not in the samples of other diseases and those of healthy subjects. The level of PADI4 relates to the disease activity and clinical performance
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