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Fibrosis is one of the major age-related failures of mammalian regenerative processes. Instead of reconstructing or maintaining the correct form of tissue, scar-like structures are deposited, disrupting organ function. Enough of this is fatal in organs such as the heart, liver, kidney, or lungs. Rising levels of fibrosis, and particularly following trauma such as infection or structural failure of aged blood vessels, are a significant component of loss of organ function and mortality in the old. Worse, the medical community has little in the way of therapies that can treat fibrosis; those that do exist are marginal in their benefits.

Fibrosis

The causes of fibrosis are thought to be complex and tissue specific because regeneration is complex and tissue specific. Considered at the high level, it is a coordinated dance carried out between stem and progenitor cells of various types, the somatic cells already present in the tissue to be worked on, and immune cells, with many and varied signals passing back and forth between all of these types. The lower level details vary considerably by tissue type and structure.

stemprogenitorsomatic cellsimmune cells

In recent years, however, investigation of senescent cells – and the ability to slow aging by targeted removal of those cells

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