Summary

Acute kidney injury (AKI) is characterised by a rapid decline in renal function and remains a significant cause of morbidity and mortality worldwide. MicroRNAs – small non-coding RNA molecules that regulate gene expression post-transcriptionally – have emerged as critical modulators of key pathways in AKI, including inflammation, cell death and tissue repair. Dysregulated microRNA profiles have been linked to tubular epithelial apoptosis, interstitial inflammation and maladaptive fibrotic responses. Conversely, certain microRNAs exert protective effects by limiting oxidative stress, attenuating pro-inflammatory cascades and promoting regenerative processes. Beyond their mechanistic roles, microRNAs circulate in blood and urine within extracellular vesicles or bound to proteins, offering a reservoir of potential biomarkers for early detection and risk stratification. Experimental modulation of specific microRNAs has demonstrated improved renal outcomes in preclinical models, suggesting novel therapeutic avenues to complement existing supportive measures.

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MicroRNA Modulation in Acute Kidney Injury publication trend

The graph below shows the total number of articles in microrna modulation in acute kidney injury across all publications each year (not limited to Nature Index journals).

Technical terms

MicroRNA: Small non-coding RNA molecule (≈22 nucleotides) that regulates gene expression by binding to target messenger RNAs, leading to translational repression or degradation.

Pyroptosis: Inflammatory form of programmed cell death characterised by cellular swelling, membrane pore formation and release of pro-inflammatory cytokines.

Ischaemia–Reperfusion Injury: Tissue damage caused by the return of blood flow after a period of oxygen deprivation, triggering oxidative stress and inflammation.

Exosome: Extracellular vesicle (30–150 nm) released by cells, carrying proteins, lipids and nucleic acids, including microRNAs, as mediators of intercellular communication.

Biomarker: Measurable indicator of a biological state or condition, used for diagnosis, prognosis or monitoring therapeutic response.

References

  1. Connexin32 gap junction channels deliver miR155-3p to mediate pyroptosis in renal ischemia-reperfusion injury. Cell Communication and Signaling (2024).
  2. Transcriptome-based exploration of potential molecular targets and mechanisms of selenomethionine in alleviating renal ischemia–reperfusion injury. Clinical Science (2023).
  3. Discovery and validation of miR-452 as an effective biomarker for acute kidney injury in sepsis. Theranostics (2020).
  4. MicroRNAs in acute kidney injury. Human Genomics (2016).

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