Systemic sclerosis is a connective tissue disease characterized by excessive collagen deposition, leading to progressive fibrosis of the skin and internal organs such as the GI tract, lungs, heart, and kidneys. It affects approximately 1.47 million people globally. Skin thickening over the digits, limbs, and trunk can cause sclerodactyly, joint contractures, and ischemic ulcers, later progressing to skin atrophy. In diffuse systemic sclerosis, an unknown trigger activates CD4⁺ T cells and B cells, resulting in autoantibody production (anti-topoisomerase I) and the release of cytokines and growth factors. This stimulates fibroblasts, leading to excessive collagen and ECM accumulation, causing widespread tissue fibrosis. Chronic inflammation and vascular injury perpetuate this process, creating a vicious cycle of tissue damage that defines the systemic nature of the disease. Scleroderma treatment remains challenging due to limited FDA approved options that only manage symptoms and slow progression, without targeting the underlying collagen overproduction.