Piezo1-Mediated Ferroptosis Delays Wound Healing in Aging Mice by Regulating the Transcriptional Activity of SLC7A11 through Activating Transcription Factor 3.

Chen Jin, Du-Piao Zhang, Zhen Lin, Yu-Zhe Lin, Yi-Feng Shi, Xiao-Yu Dong, Meng-Qi Jin, Fu-Qiang Song, Si-Ting Du, Yan-Zhen Feng, Lin-Yuan Jiang, Xiao-Qiong Jiang, Abdullah Al Mamun, Zi-Miao Chen, Jian Wang, Keqing Shi, Ren-Wen Wan, Zhi-Wen Luo, Zheng-Lin Li, Lei Yang, Jian Xiao

Department of Wound Healing, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325015, China.Department of Wound Healing, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325015, China. · pubmed

Paper

Abstract

Ferroptosis plays a role in wound healing during the maturation of senescent endothelial cells. This study explores the modulation of ferroptosis in senescent human umbilical vein endothelial cells (HUVECs) and wound-healing processes by Piezo1 activation at the molecular, cellular, and tissue levels. Elevated Piezo1 expression was observed in HUVECs treated with the senescence inducer doxorubicin (Doxo) and the ferroptosis inducer erastin and in aged wound tissue. Pharmacological inhibition or knockdown of Piezo1 protected senescent HUVECs and aged wound tissue from ferroptosis. Additionally, Piezo1 channel activity was found to promote ferroptosis in senescent HUVECs by increasing intracellular Ca

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Research summary

The paper claims that Piezo1-mediated ferroptosis delays wound healing in aging mice by regulating the transcriptional activity of SLC7A11 through activating transcription factor 3. This research is relevant as it investigates the mechanisms underlying wound healing in the context of aging, focusing on a potential pathway that could influence longevity and age-related tissue repair processes.

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