Evidence map›Paper›PMID 41637033›Full record

ReviewCurrent medical science2026

Lactate and Acidification: Emerging Metabolic Regulators of Osteoarthritis.

Yan-Hong Lin, Yi-Hua Chen, Tai-Ran Zhu, Jing Si, Yu-Fei Cao, Shuang Lv, Guang-Fan Chi

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current medical science, 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.

Yan-Hong LinThe Key Laboratory of Pathobiology of the Ministry of Education, College of Basic Medical Sciences, Jilin University, Changchun, 130021, China.
Yi-Hua ChenThe Key Laboratory of Pathobiology of the Ministry of Education, College of Basic Medical Sciences, Jilin University, Changchun, 130021, China.
Tai-Ran ZhuThe Key Laboratory of Pathobiology of the Ministry of Education, College of Basic Medical Sciences, Jilin University, Changchun, 130021, China.
Jing SiThe Key Laboratory of Pathobiology of the Ministry of Education, College of Basic Medical Sciences, Jilin University, Changchun, 130021, China.
Yu-Fei CaoThe Key Laboratory of Pathobiology of the Ministry of Education, College of Basic Medical Sciences, Jilin University, Changchun, 130021, China.
Shuang LvThe Key Laboratory of Pathobiology of the Ministry of Education, College of Basic Medical Sciences, Jilin University, Changchun, 130021, China. lvshuang@jlu.edu.cn.
Guang-Fan ChiThe Key Laboratory of Pathobiology of the Ministry of Education, College of Basic Medical Sciences, Jilin University, Changchun, 130021, China. guangfan130@jlu.edu.cn.ORCID http://orcid.org/0000-0001-7096-9106

Funding

Jilin Province Health Science and Technology Capacity Enhancement Program 2025WS-KA017National Natural Science Foundation of China 81870974National Natural Science Foundation of China 82271425
6 · The paper itself

Abstract

Osteoarthritis (OA) is a prevalent degenerative and inflammatory disease posing a significant financial and medical burden on patients and society. Lactic acid, the terminal metabolite of glycolysis, is recognized as a pivotal signaling molecule governing diverse physiological and pathological processes, particularly in cancer and inflammatory diseases. Emerging evidence suggests that metabolic disorders are closely associated with OA, which may provide a metabolic lens for further exploring its mechanisms. Glycolytic reprogramming is now recognized as a hallmark of OA, leading to the pronounced accumulation of lactic acid within the joint microenvironment. This review synthesizes current evidence to elucidate the role of lactic acid in OA pathogenesis. We summarize the mechanism of glycolytic reprogramming in chondrocytes and macrophages under pathological conditions. Furthermore, we demonstrate that lactic acid exacerbates cartilage degeneration while simultaneously promoting inflammation resolution. These dual roles are mediated by extracellular acidification, HCAR1, and lactylation. Given that duality, we suggest that redirecting lactate flux presents considerable potential as a therapeutic approach for the prevention and management of OA.

Indexed as

Lactic AcidOsteoarthritisAnimalsChondrocytesGlycolysisHumansHydrogen-Ion ConcentrationMacrophagesMetabolic ReprogrammingLactic AcidChondrocytesExtracellular acidificationHydroxycarboxylic acid receptor 1 (HCAR1)LactylationMacrophagesMetabolic reprogrammingOsteoarthritis

Identifiers

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.