Apoptosis, Pyroptosis, and Necroptosis (PANoptosis) may be Present in Renal Ischemic Injury

Emerging evidence suggests that a novel inflammatory programmed cell death pathway, PANoptosis-entailing the co-activation of apoptosis, pyroptosis, and necroptosis-may contribute to renal ischemic injury. While growing research implicates PANoptosis in the pathogenesis of diverse ischemic conditions, its specific role in AKI has not been thoroughly elucidated.

To test whether PANoptosis exists in renal ischemia diseases, we screened renal ischemia injury involving apoptosis, pyroptosis, and necroptosis as the research model and analyzed the data. Meanwhile, we detected the expression of several marker proteins (cleaved caspase-3, p-MLKL, NLRP3, and GSDMD) in HK-2 cells following ischemic injury.

The bibliometric results indicate that there is a large number of studies on apoptosis, pyroptosis, and necroptosis in cell and animal models simulating renal ischemia-reperfusion injury. Meanwhile, the experimental results show that in the ischemia-reperfusion injury model of HK-2 cells, the expression levels of key molecules involved in apoptosis, pyroptosis, and necroptosis change.

Our results demonstrate the involvement of PANoptosis in renal ischemic injury, offering a basis for targeted therapies against renal ischemia-related diseases and supporting the development of PANoptosis inhibitors.

Collectively, our findings indicate that a PANoptosis-like cell death process occurs in renal ischemic injury.