ABSTRACT Sepsis‐associated acute kidney injury (SA‐AKI) is a significant form of organ dysfunction that affects a substantial proportion of patients with sepsis, contributing to increased mortality. However, the potential mechanisms underlying SA‐AKI remain poorly understood. In this study, we identified Rab27a as a critical factor in regulating SA‐AKI, with its upregulated expression both in vitro and in vivo. The silence of Rab27a mitigated LPS‐induced injury and mitochondrial dysfunction in HK‐2 cells, leading to enhanced cell migration and functional improvement. Notably, the protective effects of Rab27a knockdown were reversed upon silencing PPAR‐γ, highlighting a potential correlation between these proteins. Furthermore, a significant interaction between PPAR‐γ and AMPK‐α1 was observed following Rab27a knockdown in RTECs during SA‐AKI. In conclusion, we demonstrated that Rab27a served as a key mediator in the pathogenesis of SA‐AKI, influencing RTEC function and mitochondrial integrity.
Mao et al. (Thu,) studied this question.