High-salt diets may increase both hypertension and risk of cardiovascular diseases. Although high-salt diets can result in hypertension and impaired vascular function, the molecular mechanisms underlying these dysfunctions are not fully known. Thus, the aims of the present study were to identify key proteins and their signaling pathways and associated molecular mechanisms that may contribute to, as well as be potential biomarkers of, the pathogenesis of hypertension-related cardiovascular diseases. To that end, the present study identified and quantitated serum proteins that were differentially expressed in male rats fed regular chow (n = 4) and those fed a high-salt diet (n = 4) to induce hypertension. The serum was collected from both groups, and the proteins differentially expressed in the serum were identified and quantitated using isobaric tags for relative and absolute quantitation combined with liquid chromatography-tandem mass spectrometry. Of 396 identified proteins, 24 were differentially expressed between the groups: 19 proteins were significantly (P < 0.05) upregulated (> 1.2 fold change), and 5 were significantly downregulated (< 0.8 fold change). Gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses indicated that these differentially expressed proteins may contribute to cardiovascular diseases via the roles they play in endothelial function, vascular remodeling, the coagulation cascade, and the complement system. In addition, phagosome processes and the integrin-associated focal adhesion signaling pathway were determined to be potential underlying molecular mechanisms. The key proteins identified in this study warrant further development as new therapeutic targets or biomarkers of cardiovascular diseases associated with high-salt diet-induced hypertension.
ABSTRACT Objectives Baker’s cyst (BC) is a complex complication of rheumatoid arthritis (RA), with a poor prognosis. This paper aimed to analyse the clinical features and risk factors for BC in patients with RA to assist clinicians in early warning and appropriate action. Methods The clinical features of the hospitalized RA patients with knee affected were analysed retrospectively. The R software was used for the statistical analysis, while logistic regression analyses were used to determine independent risk factors. Results A total of 367 RA patients with knee affected were studied, and BC was diagnosed in 15.3% of them. The BC group exhibited a higher proportion of knee-only affected than the non-BC group (P < .05), while the attributes linked to disease activity exhibited no disparity. Logistic regression analyses selected two independent risk factors for BC: knee-only affected and anaemia. A total of 26.8% of patients with BC developed rupture, exhibiting a higher proportion of knee-only affected (P < .05), compared to those unruptured. Conclusions The occurrence and rupture of BC in RA patients were significantly related to local inflammation, but not to systemic one. Incorporating local treatment may be a more advantageous option compared to solely relying on systemic therapy.
The pathology of cerebrovascular disorders, such as hypertension, is associated with genetic changes and dysfunction of basilar artery smooth muscle cells (BASMCs). Long-term high-salt diets have been associated with the development of hypertension. However, the molecular mechanisms underlying salt-sensitive hypertension-induced BASMC modifications have not been well defined, especially at the level of variations in gene transcription. Here, we utilized high-throughput sequencing and subsequent signaling pathway analyses to find a two–fold change or greater upregulated expression of 203 transcripts and downregulated expression of 165 transcripts in BASMCs derived from rats fed a high-salt diet compared with those from control rats. These differentially expressed transcripts were enriched in pathways involved in cellular, morphological, and structural plasticity, autophagy, and endocrine regulation. These transcripts changes in the BASMCs derived from high-salt intake–induced hypertensive rats may provide critical information about multiple cellular processes and biological functions that occur during the development of cerebrovascular disorders and provide potential new targets to help control or block the development of hypertension.
The heterogeneity of ovarian mesenchymal/stromal cells has just been revealed in both mice and humans. However, it remains unclear about the cellular development trace and the intercellular communication network in the whole life of the ovary. In the study, we integrated ours and published single-cell RNA sequencing data from E11.5 (embryonic day 11.5) until M12 (12-month-old) ovaries to show the dynamics of somatic cells along the developmental timeline. The intercellular crosstalk among somatic cell types was depicted with collagen signaling pathway as the most outgoing signals from stromal cells. We identified mesenchymal progenitor cells (CD24+) as the origin of stromal cells. Although their numbers decreased significantly in adults, the cells served as the major signal sender until ovarian senescence. Moreover, the ovarian injury could activate these stem cells and induce stroma remodeling in the aged ovary. Thus, mesenchymal progenitor cells may represent a new strategy to delay ovarian aging in the future.
Patients with moyamoya disease (MMD) or intracranial atherosclerotic disease (ICAD) experience similar cerebral ischaemic events. However, MMD patients show greater angiogenesis and arteriogenesis, which play crucial roles in collateral circulation development to enhance clinical prognosis and outcome. Apelins have been associated with angiogenesis and arteriogenesis. Therefore, the aim of the present study was to determine whether apelin levels were higher in patients with MMD than in patients with ICAD or in healthy controls. We compared plasma apelin levels in 29 patients with MMD, 82 patients with ICAD, and 25 healthy participants. Twelve-hour fasting blood samples were collected and analysed using commercially available kits. Univariate analyses indicated that compared with the ICAD and healthy control groups, the MMD group had higher apelin-12, apelin-13, apelin-36, and nitric oxide levels. Binary logistic regression analyses further showed that the plasma apelin-12 level was substantially higher in MMD patients than in ICAD patients. Patients with MMD were also differentiated from patients with ICAD by their mean ages, with the former being younger. Therefore, the plasma apelin-12 level is a potential diagnostic marker for differentiating MMD and ICAD and may provide a treatment strategy for enhancing collateral circulation development and clinical prognosis and outcome.
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