2. Academic Validation
  3. Sustained activation of NLRP3 inflammasome contributes to delayed wound healing in aged mice

Sustained activation of NLRP3 inflammasome contributes to delayed wound healing in aged mice

  • Int Immunopharmacol. 2023 Feb 10;116:109828. doi: 10.1016/j.intimp.2023.109828.
Haiyun Li 1,  Zhanqi Wang 1,  Feng Zhou 1,  Guorui Zhang 1,  Xuan Feng 1,  Yi Xiong 1,  Yingying Wu 2
Affiliations

Affiliations

  • 1 Department of Oral Implantology & National Clinical Research Center for Oral Diseases & State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
  • 2 Department of Oral Implantology & National Clinical Research Center for Oral Diseases & State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China. Electronic address: [email protected].
PMID: 36774855 DOI: 10.1016/j.intimp.2023.109828
Abstract

The cutaneous wounds in the elderly heal poorly, resulting in medical and economic burdens posed by defect repairing. Age-related delayed wound healing is associated with persistent inflammation and insufficient ECM deposition. The NLRP3 inflammasome has been proven to be a critical regulator of age-related inflammatory diseases, as well as impaired wound healing. Here, we create a 6 mm full-thickness cutaneous wound on the back of young and aged mice. Compared with young mice, aged counterparts display a retardation in wound healing, accompanied by increased activation of NLRP3 inflammasome. The application of the NLRP3 Inhibitor (MCC950) ameliorates wound healing in aged mice. MCC950 inhibits sustained inflammation and reduces pyroptotic cell death in fibroblasts by blocking the abnormal activation of the NLRP3 inflammasome. Our findings illuminate that the NLRP3 inflammasome is a previously unrecognized regulator of aged wound healing and may be a potential target for the therapeutic strategy of delayed wound healing with aging.

Keywords

Aging; Fibroblast; NLRP3 inflammasome; Wound healing.

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