Evidence map›Paper›PMID 42683221›Full record

ReviewFrontiers in immunology2026

NLRP3 inflammasome in acute kidney injury: molecular mechanisms, post-translational regulation, and immunotherapeutic potential.

Mingru Ma, Manling Zhang, Hongfei Sun, Xinran Xie, Xudong Guo, Hongbin Li, Yong Jin

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Mingru Ma *Inner Mongolia Key Laboratory for Pathogenesis and Diagnosis of Rheumatic and Autoimmune Diseases, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China.
Manling Zhang *Inner Mongolia Key Laboratory for Pathogenesis and Diagnosis of Rheumatic and Autoimmune Diseases, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China.
Hongfei SunInner Mongolia Key Laboratory for Pathogenesis and Diagnosis of Rheumatic and Autoimmune Diseases, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China.
Xinran XieSchool of Basic Medicine Sciences, Inner Mongolia Medical University, Hohhot, China.
Xudong GuoThe State Key Laboratory of Reproductive Regulation and Breeding of Grassland Livestock, College of Life Science, Inner Mongolia University, Hohhot, China.
Hongbin LiInner Mongolia Key Laboratory for Pathogenesis and Diagnosis of Rheumatic and Autoimmune Diseases, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China.
Yong JinInner Mongolia Key Laboratory for Pathogenesis and Diagnosis of Rheumatic and Autoimmune Diseases, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute kidney injury (AKI) is a critical clinical syndrome characterized by a rapid decline in renal function. Dysregulated inflammatory responses play a crucial role in its pathogenesis, contributing to high patient mortality and a tendency to progress to chronic kidney disease (CKD). As a crucial sensor of the innate immune system, the NLRP3 inflammasome participates in the occurrence and development of AKI and its transition to CKD by activating caspase-1, promoting the maturation of IL-1β/IL-18, and inducing pyroptosis. This review elucidates the molecular composition of the NLRP3 inflammasome, its canonical and non-canonical activation pathways, and, for the first time, integrates the critical roles of post-translational modifications-including ubiquitination, phosphorylation, acetylation, SUMOylation, and palmitoylation-in regulating its activation, as well as their specific activation mechanisms across distinct subtypes of AKI. The specific mechanisms and pathological significance of the NLRP3 inflammasome in ischemia-reperfusion, sepsis-associated, and contrast-induced AKI were analyzed. Furthermore, we summarize current interventional strategies targeting the NLRP3 inflammasome and its upstream/downstream molecules, including direct inhibitors, mitophagy inducers, K

Indexed as

Acute Kidney InjuryImmunotherapyInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinProtein Processing, Post-TranslationalAnimalsHumansInflammasomesNLR Family, Pyrin Domain-Containing 3 Proteinacute kidney injurymolecular mechanismsNLRP3 inflammasomepost-translational modificationstargeted therapy

Identifiers

PMID42683221
PMCPMC13531185

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.