Asset Details
Do you wish to reserve the book?
Mitigating Pro‐Inflammatory SASP and DAMP With Urolithin A: A Novel Senomorphic Strategy
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Mitigating Pro‐Inflammatory SASP and DAMP With Urolithin A: A Novel Senomorphic Strategy
Do you wish to request the book?
Mitigating Pro‐Inflammatory SASP and DAMP With Urolithin A: A Novel Senomorphic Strategy
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Mitigating Pro‐Inflammatory SASP and DAMP With Urolithin A: A Novel Senomorphic Strategy
2025
Overview
ABSTRACT
Senescent cells are known to contribute to aging and age‐related diseases. One key way they influence aging is by secreting senescence‐associated secretory phenotype (SASP) factors along with several damage‐associated molecular pattern (DAMP) molecules. Consequently, inhibiting SASP and DAMP signaling (senomorphics) has emerged as a therapeutic strategy. Urolithin A (UA), a gut‐derived metabolite produced from ellagitannins and ellagic acid found in berries, nuts, and pomegranates, has demonstrated potent anti‐inflammatory properties and protective effects against aging and age‐related conditions in experimental models. Here we demonstrate that UA lowers the expression and release of pro‐inflammatory SASP and DAMP factors, at least in part, by downregulating cytosolic DNA release and subsequent decrease in cGAS‐STING signaling.
Senescent cells accumulate extranuclear DNA fragments that are recognized by the cyclic GMP‐AMP synthase (cGAS) and its effector protein stimulator of interferon genes (STING), which promotes expression of SASP and DAMP genes by inducing nuclear factor‐kappa B (NF‐κB) and IFN regulatory factor 3 (IRF3) translocation. UA inhibits this process by preventing cytosolic DNA leakage and reducing cGAS‐STING signaling.
Publisher
John Wiley & Sons, Inc
