Systemic Sclerosis: Cellular Mechanisms, Innovative Diagnostics and Advanced Therapeutics

Dear Colleagues,

Systemic sclerosis (SSc) is a rare, complex autoimmune disease driven by profound immune dysregulation, vascular dysfunction, and aberrant cellular responses that result in progressive fibrosis of the skin and multiple organs. At the cellular level, fibroblast activation and transdifferentiation into myofibroblasts, mediated by cytokines, chemokines, and growth factors, play central roles in excessive extracellular matrix (ECM) deposition. Persistent activation and survival of these myofibroblasts are fueled by chronic inflammation and the release of profibrotic mediators, leading to sustained tissue fibrosis.

Another key component is endothelial cell injury, which precedes and amplifies vascular pathologies characteristic of SSc. Endothelial dysfunction results in the recruitment and activation of immune cells, further contributing to the inflammatory milieu and perpetuating fibroblast activation. Multiple cell types, including tissue resident fibroblasts, circulating fibrocytes, perivascular cells, and even transdifferentiated epithelial or adipose cells, serve as sources of activated myofibroblasts within affected tissues.

Distinct molecular pathways, such as alterations in gene regulation by non-coding RNAs, oxidative stress, and disrupted apoptotic mechanisms, converge on these cellular processes, highlighting the complexity of SSc pathogenesis. Understanding the interplay between immune cells, fibroblasts, and the endothelium is crucial for identifying mechanistically targeted therapies. This Special Issue invites research focused on the cellular and molecular mechanisms—specifically, fibroblast activation, immune cell interplay, and endothelial injury—that drive disease progression and inform innovative diagnostic, biomarker, and therapeutic strategies.

Dr. Muhammad Soyfoo
Guest Editor

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