Evidence map›Paper›PMID 40012230›Full record

ReviewRenal failure2025

Lactate metabolism and lactylation in kidney diseases: insights into mechanisms and therapeutic opportunities.

Yuhua Cheng, Linjuan Guo

Abstract readReview
In one paragraph

Review in Renal failure, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing 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

30 citing papers in PubMed.

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  19. Lactate Metabolism and Protein Lactylation in Diabetic Kidney Disease: A Narrative Review.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026
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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

2 authors.

Yuhua ChengDepartment of Nephrology, Affiliated Hospital of Jiujiang University, Jiujiang, Jiangxi, China.
Linjuan GuoDepartment of Cardiology, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang, Jiangxi, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The kidney is essential for lactate metabolism. Under normal conditions, the renal cortex mainly absorbs and metabolizes lactate, with minimal amounts excreted in urine. This process is part of a glucose-lactate recycling system between the cortex and medulla. In conditions such as acute kidney injury (AKI) and diabetic kidney disease (DKD), the kidney's ability to metabolize lactate is impaired, leading to lactate accumulation and exacerbated renal dysfunction. Novel post-translational modifications, such as lactylation, are critical in kidney disease pathophysiology by modulating gene transcription, protein function, and cellular metabolism. Lactylation is involved in inflammatory responses and tumor promotion in AKI, mitochondrial dysfunction in DKD, and tumor progression in clear cell renal cell carcinoma (ccRCC). The lactate-lactylation axis is central to the Warburg effect in ccRCC, where tumor cells preferentially rely on glycolysis rather than oxidative phosphorylation. Understanding the mechanisms of lactate metabolism and lactylation in kidney diseases may offer new therapeutic strategies. This review examines the role of lactate esters, especially lactylation, in kidney diseases, with a focus on their regulatory mechanisms and potential as therapeutic targets.

Indexed as

Acute Kidney InjuryDiabetic NephropathiesKidneyLactic AcidAnimalsCarcinoma, Renal CellGlycolysisHumansKidney NeoplasmsProtein Processing, Post-TranslationalLactic Acidacute kidney injuryclear cell renal cell carcinomadiabetic kidney diseaseLactate metabolismlactylation

Identifiers

PMID40012230
PMCPMC11869332

What OpenQuestion holds

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Registered trials

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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 OpenQuestion graph.