Circular RNA (circRNA), classified as a type of non‐coding RNA, has gained significant attention in the field of biology due to its distinctive ring structure and functional properties. Recent research has provided evidence that specific circRNAs have the ability to modulate disease progression through diverse mechanisms, one of which is by regulating cellular ferroptosis. Ferroptosis is a form of regulated cell death that is driven by iron dependency and lipid peroxidation, and extensive investigations have revealed a relationship between ferroptosis and disease development. In addition to evidence that both circRNAs and ferroptosis exert critical roles in disease progression, circRNAs have also been shown to actively mediate the process of ferroptosis. The relationship between circRNAs and ferroptosis therefore influences disease progression and offers novel targets for disease treatment. By directly or indirectly modulating the expression of circRNAs that regulate the expression of ferroptosis‐related proteins, it may be possible to impact disease progression by promoting or inhibiting ferroptosis. Current research indicates such approaches may hold significant value in a wide variety of common diseases across physiological systems. This review comprehensively summarizes the findings of recent studies investigating the roles of circRNAs in the regulation of ferroptosis in various diseases.

Competitive endogenous RNA regulation suggests an intricate network of all transcriptional RNAs that have the function of repressing miRNA function and regulating mRNA expression. Today, the specific ceRNA regulatory mechanisms of lncRNA–miRNA–mRNA in patients who have diabetes mellitus (DM) and myocardial infarction (MI) are still unknown. Two data sets, GSE34198 and GSE112690, were rooted in the Gene Expression Omnibus database to search for changes of lncRNA, miRNA, and mRNA in MI patients with diabetes. Weighted gene correlation network analysis (WGCNA) was used to identify the modules related to the development of diabetes in patients with MI. Target genes of miRNAs were predicted using miRWalk, TargetScan, mirDB, RNA22, and miRanda. Then, functional and enrichment analyses were performed to build the lncRNA–miRNA–mRNA interaction network. We built ceRNA regulatory networks with three lncRNAs, two miRNAs, and nine mRNAs. Differentially expressed genes enriched in biological process, including neutrophil activation, refer to immune response and positive system of defense feedback. Besides, there is significant enrichment in molecular function of calcium toll−like receptor binding, icosanoid binding, RAGE receptor binding, and arachidonic acid binding. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis enriched differentially expressed genes (DEGs) in pathways that were well known in MI, indicating inflammation and immune response. Pathways associated with diabetes were also significantly enriched. We confirmed significantly altered lncRNA, miRNA, and mRNA in MI patients with diabetes, which might serve as biomarkers for the progress and development of diabetic cardiovascular diseases. We constructed a ceRNA regulatory network of lncRNA–miRNA–mRNA, which will enable us to understand the novel molecular mechanisms included in the initiation, progression, and interaction between DM and MI, laying the foundation for clinical diagnosis and treatment.

Introduction: Accurately differentiating benign and malignant lesions is essential for treatment. We aimed to determine differences in urine proteomics between papillary thyroid carcinomas (PTCs) and benign thyroid nodules (BTNs) and identify biomarkers for the differential diagnosis of these diseases.Methods: We collected 155 specimens. In the discovery group, 30 PTC and 31 BTN specimens were quantitatively compared using liquid chromatography-tandem mass spectrometry (MS). The diagnostic value of each significantly altered protein was calculated in the MS validation comprising 11 PTC and 10 BTN samples. Ultimately, 36 BTN and 37 PTC specimens were used for ELISA validation.Results and discussion: Overall, 2,479 proteins were used for quantitative analysis. Compared with benign nodules, papillary carcinomas showed significant increases and decreases in the levels of 169 and 27 proteins, respectively. Neck and thyroid tumors were enriched in the disease or function category. More than 100 proteins showed good performance in the area under the receiver operating characteristic curve (>0.8) upon MS validation. Semaphorin-6D showed good performance (AUC = 0.763) in ELISA validation. Urine proteomics is an effective diagnostic tool for distinguishing benign and malignant thyroid diseases. Semaphorin-6D may serve as a disease marker for large-scale validation and use. Additionally, this study identified potential biomarkers that warrant further investigation.

Diabetic peripheral neuropathy (DPN) is a common complication of diabetes and there are currently no biomarkers for DPN in clinical practice. The objective of this study was to explore the diagnostic value of urine for diseases and discover potential markers. Urinary proteomics was used to analyze urine samples from patients with DPN and healthy individuals. Quantitative analysis of mass spectrometry data was performed using both group‐based and paired individual analysis strategies. A total of 2611 proteins were identified, of which 1759 were quantifiable, and 312 proteins showed significant differences (fold change > 2, adjusted p value < 0.01), with 239 decreased and 73 increased. A random grouping cross‐validation strategy was employed to evaluate the differentially expressed proteins, ensuring that the probability of random differences was less than 10%. Unsupervised clustering analysis of urinary proteomes among groups could distinguish most specimens. The most enriched GO biological processes were cytoplasmic translation, translation, exocytosis, chaperone‐mediated protein folding and immunoglobulin‐mediated immune response. The most significant KEGG signaling pathways were ribosome, coronavirus disease (COVID‐19), and metabolic pathways. Furthermore, some differentially expressed proteins were linked to the pathogenesis of diabetes, whereas others were associated with nerve damage. These molecules could serve as potential diagnostic and therapeutic biomarkers; some differential proteins have not yet been reported to be associated with DPN, providing clues for further research on their functions.