Researchers reviewed recent research data on tissue remodeling in the context of lung disorders. Cell differentiation, sensitivity to growth factors, hormones, or environmental variables, and extracellular matrix composition are all found to be a part of tissue remodeling. Researchers wanted to determine if one trigger can set them all off, or are all regulated separately? New data from clinical and experimental research supported the idea that remodeling vulnerability can be established early in childhood and then reactivated later in life by environmental stimuli. TGF- plays a crucial role in the pathophysiology of remodeling and fibrosis, according to several studies. The activation routes and end-effects of TGF-activation, on the other hand, appear to be illness and effector cell-specific patterns. Existing animal models do not accurately reflect human illness and must be developed further.
TGF-‘s important function in pathogenic pathways that lead to remodeling and fibrosis has been proven once more. However, it is still unknown why TGF- is activated, as well as its disease and cell type-specific mechanisms of action. Redefining the phrase ’tissue remodeling’ in disease and cell type-specific fashion should be examined based on clinical facts.
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