GSDME-controlled pyroptosis promotes muscle repair by coordinating tissue resident macrophages and fibro-adipogenic progenitors [RNA-seq]

GSDME (Gasdermin E) is a critical protein known for its role in pyroptosis, a form of programmed cell death associated with inflammation. We demonstrated that GSDME as a crucial mediator in muscle repair, particularly in the context of muscle damage induced by cardiotoxin (CTX). Specifically, we found that GSDME-controlled pyroptosis promotes muscle repair by coordinating the activities of tissue-resident macrophages and fibro-adipogenic progenitors (FAPs). Overall design: To simulate a muscle injury repair model, CTX (cardiotoxin) was injected into the thigh muscles of wild-type (WT) mice. Samples were collected from both the injection group and the control (unloaded) group to assess the effects of the model.To explore the function of the Gsdme, we conducted detailed experiments in both WT and knockout (KO) mice. Gastrocnemius muscles were harvested from WT injection groups and KO injection groups at four different time points: Day 1, Day 4, Day 7, and Day 14 post-injection. Each group included biological triplicates. These samples were then subjected to RNA sequencing (RNA-seq) analysis.