Abstract
Background: miR-210, a key hypoxamiR, regulates hypoxia and inflammation-linked hypoxia. Systemic lupus erythematosus (SLE), a chronic autoimmune disease, is responsible for many pathological disorders, including photosensitivity. Objective: This study aimed to find the correlation between circulating miR-210/HIF-1 alpha levels and photosensitivity in SLE patients and other SLE-associated pathological complications in a single-center case-control study. Methods: The study population comprised 104 SLE Egyptian patients with photosensitivity, 32 SLE patients without photosensitivity, and 32 healthy subjects. SLE activity was assessed for all patients using the SLE Disease Activity Index (SLEDAI). Clinical complications/manifestations and hematological/serological analyses were recorded. HIF-alpha concentration was investigated by ELISA, and miR-210 expression was analyzed by qRT-PCR. Results: The results revealed that circulating miR-210 was significantly increased in the SLE/photosensitivity group versus the SLE and control groups. The additional occurrence of malar rash, oral ulcers, renal disorders, or hypertension resulted in a higher expression of miR-210. SLEDAI activity status showed no effect on miR-210. Erythrocyte sedimentation rate, white blood cells, hemoglobin, platelets, patient age, and disease duration were positively correlated with circulatory miR-210. HIF-alpha concentration was significantly induced in the SLE/photosensitivity group versus the SLE and control groups. In SLE/photosensitivity, the presence of renal disorders and hypertension resulted in the highest HIF-alpha concentrations. A strong positive correlation was recorded between HIF-alpha concentration and circulatory miR-210 in SLE/photosensitivity patients (r = 0.886). Conclusion: The dysregulation of circulating miR-210/HIF-1 alpha levels in SLE/ photosensitivity patients is controlled by the presence of additional pathological complications, and results suggest that the hypoxia pathway might interact positively with the pathogenesis and disease progression of SLE. 10.2174/1566524022666220114145220