Nowaczyk Joanna, Blicharz Leszek, Zawistowski Michał, Sikora Mariusz, Zaremba Michał, Czuwara Joanna, Rudnicka Lidia
Department of Dermatology, Medical University of Warsaw, 02-091 Warsaw, Poland.
National Institute of Geriatrics, Rheumatology and Rehabilitation, 02-637 Warsaw, Poland.
Diagnostics (Basel). 2023 Feb 23;13(5):848. doi: 10.3390/diagnostics13050848.
Systemic sclerosis (SSc) is a connective tissue disease manifesting with progressive fibrosis of the skin and internal organs. Its pathogenesis is strictly associated with vascular disfunction and damage. Salusin-α and salusin-β, endogenous peptides regulating secretion of pro-inflammatory cytokines and vascular smooth muscle proliferation, may potentially play a role in SSc pathogenesis. The aim of this study was to assess the concentration of salusins in sera of patients with SSc and healthy controls and to evaluate correlations between the salusins levels and selected clinical parameters within the study group. 48 patients with SSc (44 women; mean age, 56.4, standard deviation, 11.4) and 25 adult healthy volunteers (25 women; mean age, 55.2, standard deviation, 11.2) were enrolled. All patients with SSc were treated with vasodilators and twenty-seven of them (56%) also received immunosuppressive therapy. Circulating salusin-α was significantly elevated in patients with SSc in comparison to healthy controls (U = 350.5, = 0.004). Patients with SSc receiving immunosuppression had higher serum salusin-α concentrations compared with those without immunosuppressive therapy (U = 176.0, = 0.026). No correlation was observed between salusins concentrations and skin or internal organ involvement parameters. Salusin-α, a bioactive peptide mitigating the endothelial disfunction, was elevated in patients with systemic sclerosis receiving vasodilators and immunosuppressants. Increased salusin-α concertation may be associated with the initiation of atheroprotective processes in patients with SSc managed pharmacologically, which requires verification in future studies.
系统性硬化症（SSc）是一种结缔组织疾病，表现为皮肤和内脏器官的进行性纤维化。其发病机制与血管功能障碍和损伤密切相关。Salusin-α和Salusin-β是调节促炎细胞因子分泌和血管平滑肌增殖的内源性肽，可能在SSc发病机制中发挥作用。本研究的目的是评估SSc患者和健康对照者血清中Salusin的浓度，并评估研究组中Salusin水平与选定临床参数之间的相关性。招募了48例SSc患者（44例女性；平均年龄56.4岁，标准差11.4）和25名成年健康志愿者（25例女性；平均年龄55.2岁，标准差11.2）。所有SSc患者均接受血管扩张剂治疗，其中27例（56%）还接受了免疫抑制治疗。与健康对照相比，SSc患者循环中的Salusin-α显著升高（U = 350.5，P = 0.004）。接受免疫抑制的SSc患者血清Salusin-α浓度高于未接受免疫抑制治疗的患者（U = 176.0，P = 0.026）。未观察到Salusin浓度与皮肤或内脏器官受累参数之间的相关性。Salusin-α是一种减轻内皮功能障碍的生物活性肽，在接受血管扩张剂和免疫抑制剂治疗的系统性硬化症患者中升高。Salusin-α浓度升高可能与接受药物治疗的SSc患者的动脉粥样硬化保护过程的启动有关，这需要在未来的研究中进行验证。
