Scientists ID new targets to treat fibrosis, a feature of many chronic diseases

ScienceDaily | 10/4/2019 | Staff
Frost123 (Posted by) Level 3
The report, published online October 4 in the journal Nature Communications, describes in detail the novel signaling pathway by which reduced calcium uptake in mitochondria serves as the major regulator of myofibroblast differentiation and fibrosis. When mitochondrial calcium levels drop, cellular metabolism changes and a metabolite known as α-ketoglutarate is upregulated. Increased α-ketoglutarate levels in turn alter the packaging of cellular DNA, changing gene expression for the conversion of fibroblasts into fibrosis-mediating myofibroblasts.

"When fibroblast signaling alters mitochondrial calcium uptake, many metabolic changes occur to promote anabolic pathways to support the formation of these new cells and provide new sources of energy production," said John W. Elrod, PhD, Associate Professor in the Center for Translational Medicine at LKSOM, and senior investigator on the new study. "These changes are necessary for the new role of these cells to alter the cellular environment in an attempt to repair the injured tissue."

Formation - Acute - Wound - Healing - Closing

While myofibroblast formation is associated with acute wound healing -- think the closing of a cut on the skin -- the persistence of...
(Excerpt) Read more at: ScienceDaily
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