Fibrosis is a malfunction of tissue maintenance in which excessive scar-like collagen deposits disrupt tissue structure and function. This may be one of the consequences of the chronic inflammation of aging, and senescent cell accumulation is implicated in the progression of fibrosis. Researchers here show that upregulation of SIRT3 can reverse some of the disruption of cell function that causes fibrosis, resulting in improvements to health in aged mice. The approach they take is to deliver SIRT3 plasmids into the airway, where they are taken up by macrophage cells. Altered macrophage behavior as a result of increased SIRT3 expression then produces further signaling and cell behavior changes that lead to a reduction in fibrosis.
Fibrotic disorders span across multiple organ systems. A consistent pathological finding in these disorders is the accumulation of activated myofibroblasts and deposition of mature extracellular matrix in association with impaired capacity for epithelial cell regeneration. In most species and across organs in humans, regeneration and fibrosis are antagonistically and inversely related. While impaired regeneration leads to fibrosis, a skewing of the tissue repair response to fibrosis may reciprocally dampen latent regenerative capacity. Aging is known to be associated with impaired regenerative capacity, and it
Article originally posted at