BioAcyl Corp |
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| Resource type: Journal Article DOI: 10.1126/science.adp2974 ID no. (ISBN etc.): 0036-8075 BibTeX citation key: Martin2024 View all bibliographic details |
Categories: BioAcyl Corp Subcategories: Fibrosis Creators: Jenkins, Martin, Pardo-Pastor Collection: Science (New York, N.Y.) |
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| Abstract |
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Although the age of the genome gave us much insight about how our organs fail with disease, it also suggested that diseases do not arise from mutations alone; rather, they develop as we age. Here, we examine how wound healing might act to ignite disease. Wound healing works well when we are younger, repairing damage from accidents, environmental assaults, and battles with pathogens. Yet, with age and accumulation of mutations and tissue damage, the repair process can go off the rails, leading to inflammation, fibrosis, and neoplastic signalling. Here, we discuss healthy wound responses and how our bodies might misappropriate these pathways in disease. Although we focus predominantly on epithelial based (lung and skin) diseases, similar pathways might operate in cardiac, muscle, and neuronal diseases.
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