Corrigendum: JAK1/2 inhibitor baricitinib improves skin fibrosis and digital ulcers in systemic sclerosis.

[This corrects the article DOI: 10.3389/fmed.2022.

JAK1/2 Inhibitor Baricitinib Improves Skin Fibrosis and Digital Ulcers in Systemic Sclerosis.

Background: Systemic sclerosis (SSc) is a rare disabling connective tissue disease with few available treatment options. Diffuse cutaneous systemic sclerosis (dcSSc) is associated with high mortality. A previous experiment has shown that JAK2 inhibitor can significantly improve skin fibrosis in bleomycin (BLM)-induced murine model, including reducing dermal thickening and collagen accumulation.

BTXA regulates the epithelial-mesenchymal transition and autophagy of keloid fibroblasts via modulating miR-1587/miR-2392 targeted ZEB2.

Keloids are very resistant to treatment in dermatology and plastic surgical practice. The present study aimed to explore the underlying mechanism of botulinum toxin A (BTXA) treated human skin keloid fibroblasts (HSFBs) proving some new insights into keloids treatment. Expression of miR-1587 and miR-2392 were significantly down-regulated in keloid tissues and HSFBs, while the ZEB2 was a target of both and up-regulated in keloid tissues and HSFBs compared with the normal controls.