Objectives: Persistent sciatic artery (PSA) is a rare congenital malformation w which could lead to serious complications such as lower extremity ischemiais. We report the treatment of a PSA patient combined with limb ischemia. Methods: A 64-year-old man was admitted to the hospital for intermittent claudication of the right lower limb. The right ankle-brachial index (ABI) was 0.5. Computed Tomography Angiography (CTA) revealed the presence of incomplete PSA with an absence superficial femoral artery. We performed catheter-directed thrombolysis (CDT) and stenting placement for the patient. Results: The vessels were successfully opened and the claudication was resolved. However, half a year after the operation, the right PSA of the patient was occluded. Conclusion: The etiology, pathophysiology and anatomic factors should be considered in the treatment of PSA. Endovascular treatment, bypass surgery, and drug therapy should be balanced. Improper choice of any treatment regimen may result in poor prognosis.

The aging process significantly contributes to human disease, and as worldwide life expectancy increases, addressing the challenges of aging and age-related cardiovascular diseases is becoming increasingly urgent. Vascular aging is a key link between aging and the development of age-related diseases. Recent studies indicate that proprotein convertase subtilisin/kexin type 9 (PCSK9), a type of protein involved in the metabolism of lipids, is crucial in modulating vascular aging by affecting the physiological functioning of vascular cells. PCSK9 is linked to lipid metabolism and chronic inflammation and is involved in regulating senescence-related activities, including migration, proliferation, apoptosis, and differentiation. These factors contribute to the aging of vascular cells and age-related vascular diseases, including atherosclerosis, hypertension, coronary artery disease, and cerebrovascular diseases. Given its involvement in these processes, this article provides a comprehensive summary of PCSK9's regulatory functions in vascular aging, highlighting potential therapeutic targets for combating age-related cardiovascular diseases.

Background: Deep vein thrombosis (DVT) is a prevalent peripheral vascular disease. The intricate and multifaceted nature of the associated mechanisms hinders a comprehensive understanding of disease-relevant targets. This study aimed to identify and examine the most distinctive genes linked to DVT.Methods: In this study, the bulk RNA sequencing (bulk RNA-seq) analysis was conducted on whole blood samples from 11 DVT patients and six control groups. Topology analysis was performed using seven protein-protein interaction (PPI) network algorithms. The combination of weighted correlation network analysis (WGCNA) and clinical prediction models was employed to validate hub DEGs. Furthermore, single-cell RNA sequencing (scRNA-seq) was performed on peripheral blood samples from 3 DVT patients and three control groups to probe the cellular localization of target genes. Based on the same methodology as the internal test set, 12 DVT patients and six control groups were collected to construct an external test set and validated using machine learning (ML) algorithms and immunofluorescence (IF). Concurrently, the examination of the pathways in disparate cell populations was conducted on the basis of the CellChat pathway.Results: A total of 193 DEGs were identified in the internal test set. Additionally, a total of eight highly characteristic genes (including TLR1, TLR7, TLR8, CXCR4, DDX58, TNFSF10, FCGR1A and CD36) were identified by the PPI network algorithm. In accordance with the WGCNA model, the aforementioned genes were all situated within the blue core module, exhibiting a correlation coefficient of 0.84. The model demonstrated notable disparities in TLR8 (P = 0.018, AUC = 0.847), CXCR4 (P = 0.00088, AUC = 1.000), TNFSF10 (P = 0.00075, AUC = 0.958), and FCGR1A (P = 0.00022, AUC = 0.986). Furthermore, scRNA-seq demonstrated that B cells, T cells and monocytes play an active role in DVT. In the external validation set, CXCR4 was validated as a potential target by the ML algorithm and IF. In the context of the CellChat pathway, it indicated that MIF - (CD74 + CXCR4) plays a potential role.Conclusion: The findings of this study indicate that CXCR4 may serve as a potential genetic marker for DVT, with MIF - (CD74 + CXCR4) potentially implicated in the regulatory mechanisms underlying DVT.

Deep vein thrombosis (DVT) is a complex thrombotic disorder with multiple environmental and genetic determinants. Nevertheless, the intricacies of DVT regu

Deep vein thrombosis (DVT) is a prevalent peripheral vascular disease that is frequently accompanied by significant complications. However, the complexity and diversity of its pathogenesis have resulted in a lack of in-depth understanding of relevant regulatory targets. The objective of this study was to identify the highly distinctive genes associated with DVT, and to investigate their intricacies. In this study, a comprehensive transcriptomic analysis was conducted on blood samples from 4 DVT patients and 6 healthy subjects from an internal test set, employing established standard procedures. Differential (diff) circular RNAs (circRNAs), diff microRNAs (miRNAs) and diff messenger RNAs (mRNAs) associated with DVT were identified to construct a competing endogenous RNA (ceRNA) network model, and node mRNAs were identified in an external validation set (n = 14). Furthermore, a topological analysis was conducted by using 7 protein–protein interaction (PPI) network algorithms. Concurrently, AlphaFold 2 was employed for three-dimensional prediction and assessment of the molecular structure. The comparative toxicology genomics database (CTD) was employed to assess the interconnectivity between these genes. Subsequently, single-cell RNA sequencing (scRNA-seq) was conducted on blood samples from 3 DVT patients and 3 healthy subjects, following the standard protocol, to ascertain the cellular localization of gene expression and the role of core pathways. A whole-transcriptome analysis identified a total of 406 diff circRNAs, 29 diff miRNAs and 154 diff mRNAs. Concurrently, a total of 6 circRNAs, 5 miRNAs and 16 mRNAs were incorporated into the ceRNA network models (a total of 6 node mRNAs were identified differentially). A total of 5 hub genes (including JAK2, CD36, TNFSF13B, TLR7 and PARP9) were identified by 7 PPI network algorithms. The structure and function of the above genes are adequately described by the AlphaFold 2 and CTD interference scores. A total of 7 cell types were identified by scRNA-seq, and there were obvious differences in the localization of genes and the role of core pathways in different cells. JAK2, CD36, TNFSF13B, TLR7 and PARP9 were identified as potential regulatory target genes for the pathophysiological process of DVT. Additionally, hsa_circ_0095124/hsa-miR-3074-5p/TNFSF13B is a potential regulatory pathway for DVT.

Platelet function and count display robust circadian oscillations with a period of approximately 24 hours, governed by the core molecular clock and modulated by environmental factors such as light, diet, and stress. This review elaborates on three key aspects. First, platelet surface markers peak around 8–9 AM, whereas platelet count, ATP release, and aggregability reach their maximum between 3–8 PM. Mechanistically, the nuclear receptor Rev-erbα drives the morning surge in platelet reactivity and thrombosis via the OPHN-1/RhoA/ERM signaling pathway. Second, through their circadian rhythm, platelets actively participate in the pathogenesis of cardiovascular diseases, neurological disorders, and metabolic diseases. Third, circadian-targeting drugs including tasimelteon, ramelteon, agomelatine, SR9009, VTP-43742, and PF-670462 offer novel therapeutic strategies for rhythm-related disorders. This review highlights the circadian regulation of platelets as an emerging therapeutic target in human diseases.