Abstract:
:Fibrosis-related diseases carry with them a high mortality rate and their morbidity increases with age. Recent findings indicate that induced senescence in myofibroblasts can limit or reduce myocardial fibrosis, cirrhosis, and idiopathic pulmonary fibrosis, while also accelerating wound healing. However, more senescent cells are accumulated as organisms age, which exacerbates aging-related diseases. These two contradictory theories inspired us to summarize papers on the restrictive effect of senescence on fibrosis and to input the key findings into simple software that we developed to assist with data organization and presentation. In this review, we illustrate that senescent cells secrete more matrix metalloproteinases to solubilize excess collagen, while chemokines and cytokines activate immune cells to eliminate senescent cells. In the elderly, it is perhaps more effective to limit fibrosis by inducing myofibroblast senescence and then removing senescent cells that are not cleared via normal mechanisms by antisenescence therapies.
journal_name
J Cell Physioljournal_title
Journal of cellular physiologyauthors
Meng X,Wang H,Song X,Clifton AC,Xiao Jdoi
10.1002/jcp.29313subject
Has Abstractpub_date
2020-05-01 00:00:00pages
4046-4059issue
5eissn
0021-9541issn
1097-4652journal_volume
235pub_type
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