The neuropeptide cortistatin regulates dermal and pulmonary fibrosis in an experimental model of systemic sclerosis
Conclusion: We identify cortistatin as an endogenous break of skin inflammation and fibrosis. Deficiency in cortistatin could be a marker of poor-prognosis of scleroderma and associated-complications. Cortistatin-based therapies emerge as attractive candidates to treat severe forms of systemic sclerosis, and to manage fibrosis-related side effects of bleomycin-chemotherapy in oncologic patients.
Source: Neuroendocrinology - Category: Endocrinology Source Type: research
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