Cardiovascular disease is a leading cause of death in Chinese population. It is of great significance to further explore the pathogenesis of cardiovascular diseases. Ferroptosis is a recently discovered iron-dependent and non-apoptotic form of regulated cell death, which exerts a regulatory role in a variety of biological events. Some studies have shown that ferroptosis plays an important role in the development of cardiovascular diseases. According to newly scientific reports, we summarized the mechanism and regulation in ferroptosis, and reviewed the results of ferroptosis in common cardiovascular diseases such as cardiac ischemia-reperfusion/myocardial infarction, cardiomyopathy, cardiac hypertrophy, atherosclerosis and abdominal aortic aneurysm.
Vascular calcification is an active, adjustable and complex biological process. It is an independent hazard factor for cardiovascular events and there is a lack of effective treatment. As a newly discovered regulated cell death, ferroptosis is closely related to iron metabolism, lipid metabolism, glutathione metabolism and so on. In recent years, studies have shown that ferroptosis may be implicated in the occurrence and progression of vascular calcification. Based on the introduction of ferroptosis, this review will discuss the close relationship between ferroptosis and vascular calcification from intimal calcification, medial calcification and heart valve calcification, in order to provide new ideas for the prevention and treatment of vascular calcification.
Diabetic retinopathy (DR) constitutes a major retinal vascular disorder leading to blindness in adults. Current therapeutic approaches for DR exhibit certain degrees of efficacy but are constrained by a spectrum of limitations. Hence, there is a pressing need to deeply investigate the underlying pathogenesis of DR and explore novel therapeutic targets. Ferroptosis, a distinctive form of programmed cell death, has emerged as a pertinent phenomenon in recent years. Notably, ferroptosis has been implicated in the progression of DR through mechanisms involving the induction of retinal oxidative stress, provocation of anomalous retinal vascular alterations, exacerbation of retinal neural damage, and elicitation of immune dysregulation. Thus, elucidating the mechanistic role of ferroptosis in DR holds the potential to establish a robust foundational rationale. This could potentially facilitate the clinical translation of ferroptosis inhibitors as promising agents for the prevention and treatment of DR, thereby forging novel avenues in the landscape of DR management.
Ferroptosis, as a new form of programmed cell death, affects the occurrence, progression and treatment of liver cancer. In this paper, the discovery, characteristics, regulatory mechanisms, inhibitors, inducers, and detection indicators of ferroptosis were systematically summarized and analyzed, and the effects of ferroptosis on the progression, metastasis, treatment, and prognosis of liver cancer were summarized. Finally, it was concluded that targeting ferroptosis is a promising treatment strategy for liver cancer.
Objective To explore the correlation and mechanism of ferroptosis with pulmonary fibrosis. Methods Pulmonary fibrosis tissue sequencing data were obtained from Gene Expression Omnibus and FerrDb databases from January 2019 to December 2023. Differentially expressed genes (DEGs) between the normal control group and the pulmonary fibrosis group were analyzed by bioinformatic method, and DEGs related to pulmonary iron addiction were extracted. The hub genes were screened by enrichment analysis, protein-protein interaction (PPI) analysis and random forest algorithm. The mouse model of pulmonary fibrosis was made for exercise intervention, and the expression of hub genes was verified by real-time quantitative reverse transcription polymerase chain reaction. Results A comparison of 103 patients with idiopathic pulmonary fibrosis and 103 normal lung tissues showed that 13 up-regulated genes and 7 down-regulated genes were identified as ferroptosis-related DEGs. PPI results showed that there was an interaction between these ferroptosis-related genes. The Kyoto Encyclopedia of Genes and Genomes pathway enrichment and Genome Ontology enrichment analysis showed that ferroptosis-related genes were involved in organic anion transport, hypoxia response, oxygen level reduction response, hypoxia-inducible factor-1 signaling pathway, renal cell carcinoma, and arachidonic acid metabolic signaling pathway. Genes identified by PPI analysis and random forest algorithm included CAV1, NOS2, GDF15, HNF4A, and CDKN2A. Real-time fluorescence quantitative polymerase chain reaction results of mouse fibrotic lung tissue showed that compared with the exercise group, the mRNA levels of NOS2, PTGS2 and GDF15 were up-regulated and the mRNA levels of CAV1 and CDKN2A were down-regulated in the bleomycin group (P<0.05); compared with the bleomycin group, the expression of CAV1 and CDKN2A increased and the expression of NOS2, PTGS2 and GDF15 decreased in the bleomycin + exercise group (P<0.05). Conclusions Bioinformatic analysis identifies 20 potential genes associating with ferroptosis in pulmonary fibrosis. CAV1, NOS2, GDF15, and CDKN2A influence the development of pulmonary fibrosis by modulating ferroptosis. Treadmill training can reduce ferroptosis in fibrotic tissues, thereby reducing lung inflammation.