# Inflammation, cell death, and lncRNAs: unraveling the mechanisms of sepsis-associated acute kidney injury

## TL;DR

This paper reviews how inflammation, cell death, and long non-coding RNAs contribute to kidney injury in sepsis, highlighting their potential as biomarkers or treatment targets.

## Contribution

The paper provides new insights into the dual role of lncRNAs in sepsis-associated acute kidney injury and their regulatory mechanisms.

## Key findings

- lncRNAs modulate inflammation, oxidative stress, and cell death in sepsis-associated kidney injury.
- lncRNAs can act as both harmful and protective factors in renal injury, depending on the context.
- lncRNAs show promise as diagnostic biomarkers and therapeutic targets in SA-AKI.

## Abstract

Sepsis-associated acute kidney injury (SA-AKI) is a common and devastating complication of sepsis and remains a major contributor to morbidity and mortality in critically ill patients. Despite advances in supportive care, effective pharmacological therapies are still lacking, largely due to the complex and multifactorial pathogenesis of SA-AKI. Accumulating evidence indicates that dysregulated inflammation, oxidative stress, and multiple forms of programmed cell death—including apoptosis, pyroptosis, ferroptosis, and autophagy—are central drivers of renal tubular and endothelial dysfunction during sepsis. Recent studies have identified long non-coding RNAs (lncRNAs) as critical regulators of these pathogenic processes. Through competing endogenous RNA networks or direct interactions with proteins, lncRNAs modulate inflammatory signaling, oxidative stress responses, and cell fate decisions. This review summarizes current mechanistic insights into lncRNA-mediated regulatory networks in SA-AKI, highlights representative molecular axes defined in experimental models, and discusses the translational potential of lncRNAs as diagnostic biomarkers or therapeutic targets. Importantly, lncRNAs exhibit a context-dependent duality, acting as either pathogenic amplifiers or protective modulators of renal injury, underscoring both their biological complexity and clinical relevance in SA-AKI.