Ferroptosis, a type of regulated cell death driven by iron-dependent lipid peroxidation, is mainly initiated by extramitochondrial lipid peroxidation due to the accumulation of iron-dependent reactive oxygen species. Ferroptosis is a prevalent and primitive form of cell death. Numerous cellular metabolic processes regulate ferroptosis, including redox homeostasis, iron regulation, mitochondrial activity, amino acid metabolism, lipid metabolism, and various disease-related signaling pathways. Ferroptosis plays a pivotal role in cancer therapy, particularly in the eradication of aggressive malignancies resistant to conventional treatments. Multiple studies have explored the connection between ferroptosis and bladder cancer, focusing on its incidence and treatment outcomes. Several biomolecules and tumor-associated signaling pathways, such as p53, heat shock protein 1, nuclear receptor coactivator 4, RAS-RAF-MEK, phosphatidylinositol 3-kinase-AKT-mammalian target of rapamycin, and the Hippo-tafazzin signaling system, exert a moderating influence on ferroptosis in bladder cancer. Ferroptosis inducers, including erastin, artemisinin, conjugated polymer nanoparticles, and quinazolinyl-arylurea derivatives, hold promise for enhancing the effectiveness of conventional anticancer medications in bladder cancer treatment. Combining conventional therapeutic drugs and treatment methods related to ferroptosis offers a promising approach for the treatment of bladder cancer. In this review, we analyze the research on ferroptosis to augment the efficacy of bladder cancer treatment.
This study aimed to investigate the changes of follicular helper T (TFH) and follicular regulatory T (TFR) cell subpopulations in patients with non-small cell lung cancer (NSCLC) and their significance.
Peripheral blood was collected from 58 NSCLC patients at different stages and 38 healthy controls. Flow cytometry was used to detect TFH cell subpopulation based on programmed death 1 (PD-1) and inducible co-stimulator (ICOS), and TFR cell subpopulation based on cluster determinant 45RA (CD45RA) and forkhead box protein P3 (FoxP3). The levels of interleukin-10 (IL-10), interleukin-17a (IL-17a), interleukin-21 (IL-21), and transforming growth factor-β (TGF-β) in the plasma were measured, and changes in circulating B cell subsets and plasma IgG levels were also analyzed. The correlation between serum cytokeratin fragment antigen 21-1 (CYFRA 21-1) levels and TFH, TFR, or B cell subpopulations was further explored.
The TFR/TFH ratio increased significantly in NSCLC patients. The CD45RA+FoxP3int TFR subsets were increased, with their proportions increasing in stages II to III and decreasing in stage IV. PD-1+ICOS+TFH cells showed a downward trend with increasing stages. Plasma IL-21 and TGF-β concentrations were increased in NSCLC patients compared with healthy controls. Plasmablasts, plasma IgG levels, and CD45RA+FoxP3int TFR cells showed similar trends. TFH numbers and plasmablasts were positively correlated with CYFRA 21-1 in stages I–III and negatively correlated with CYFRA 21-1 in stage IV.
Circulating TFH and TFR cell subpopulations and plasmablasts dynamically change in different stages of NSCLC, which is associated with serum CYFRA 21-1 levels and reflects disease progression.
Atherosclerosis (AS) is characterized by impairment and apoptosis of endothelial cells, continuous systemic and focal inflammation and dysfunction of vascular smooth muscle cells, which is documented as the traditional cellular paradigm. However, the mechanisms appear much more complicated than we thought since a bulk of studies on efferocytosis, transdifferentiation and novel cell death forms such as ferroptosis, pyroptosis, and extracellular trap were reported. Discovery of novel pathological cellular landscapes provides a large number of therapeutic targets. On the other side, the unsatisfactory therapeutic effects of current treatment with lipid-lowering drugs as the cornerstone also restricts the efforts to reduce global AS burden. Stem cell- or nanoparticle-based strategies spurred a lot of attention due to the attractive therapeutic effects and minimized adverse effects. Given the complexity of pathological changes of AS, attempts to develop an almighty medicine based on single mechanisms could be theoretically challenging. In this review, the top stories in the cellular landscapes during the initiation and progression of AS and the therapies were summarized in an integrated perspective to facilitate efforts to develop a multi-targets strategy and fill the gap between mechanism research and clinical translation. The future challenges and improvements were also discussed.