Nephron repair: powered by anaerobic energy metabolism

Acute kidney injury (AKI) is clinically classified as abrupt organ damage that occurs within a short time period spanning a few hours or days (1). AKI commonly attacks anatomical structures called nephrons, which are tubular units responsible for conducting the essential excretory and osmoregulatory functions of the kidney. AKI frequently has fatal consequences, but this condition is highly heterogeneous and patients can exhibit partial or complete restoration of renal activities (1). There have been many critical advances in understanding the molecular basis of kidney damage and subsequent tissue regeneration in recent years (2). Despite such progress, new treatments that definitively improve outcomes for AKI patients have not been identified, and thus there remains an urgent necessity to discover useful therapeutic approaches (3). A challenge in this regard is that many aspects of renal injury and subsequent reparative and/or regenerative processes remain opaque, while others are highly controversial due to conflicting studies, such as the involvement of endogenous stem cells (2). Therefore, it is pivotal to uncover further insights into the cellular and genetic mechanisms that regulate the response to kidney injury