Journal
CELL DEATH & DISEASE
Volume 13, Issue 6, Pages -Publisher
SPRINGERNATURE
DOI: 10.1038/s41419-022-04981-9
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Funding
- Natural Science Foundation of China [81770876]
- Natural Science Foundation of Jiangsu Province [BK20191141]
- Top Talent Support Program for young and middle-aged people of Wuxi Health Committee [BJ2020044, BJ2020057, HB2020043]
- Fundamental Research Funds of Health and Family Planning Commission of Wuxi [M202024]
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Inflammation is a main feature leading to skin fibrosis, and acid-sensing ion channel 3 (ASIC3) may play a role in promoting fibrosis through regulating macrophage polarization and transforming growth factor beta 1 (TGF-beta 1). Targeting ASIC3 may be a new treatment strategy for skin fibrosis.
Inflammation is one of the main pathological features leading to skin fibrosis and a key factor leading to the progression of skin fibrosis. Acidosis caused by a decrease in extracellular pH is a sign of the inflammatory process. Acid-sensing ion channels (ASICs) are ligand-gated ion channels on the cell membrane that sense the drop in extracellular pH. The molecular mechanisms by which skin fibroblasts are regulated by acid-sensing ion channel 3 (ASIC3) remain unknown. This study investigated whether ASIC3 is related to inflammation and skin fibrosis and explored the underlying mechanisms. We demonstrate that macrophage colony-stimulating factor (M-CSF) is a direct target of ASIC3, and ASIC3 activation promotes M-CSF transcriptional regulation of macrophages for M2 polarization. The polarization of M2 macrophages transduced by the ASIC3-M-CSF signal promotes the differentiation of fibroblasts into myofibroblasts through transforming growth factor beta 1 (TGF-beta 1), thereby producing an ASIC3-M-CSF-TGF-beta 1 positive feedback loop. Targeting ASIC3 may be a new treatment strategy for skin fibrosis.
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