ISSN: 2639-216X
Authors: Bindu S*
Tissue fibrosis is a set of progressive debilitating diseases which although initiate as a normal wound healing response to an injury, end up with hyperactivated immunological state leading to overwhelming deposition of extra cellular matrix (ECM) components by activated fibroblasts. About 45% deaths in the US are attributed to fibrosis-associated organ damage [1]. Repeated cycles of tissue injury-repair cause molecular dyshomeostasis and chronic inflammation wherein the affected organs suffer stiffening, scarring and consequential functional loss. Fibrosis of major organs including lungs, heart, liver, kidney, intestine and skin largely contributes to the clinical complications of major diseases characterized by multi-organ failure. Various genetic factors are evidently linked to tissue-specific development of fibrosis in humans [2].
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