Evidence map›Paper›PMID 42742769›Full record

ReviewMolecular biology reports2026

LPA₃ signaling and biological functions: from physiological regulation to disease-targeted therapy.

Xiaomeng Li, Ruixuan Wang, Donglin Yang, Qifa Ye, Zibiao Zhong

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular biology reports, 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

5 authors.

Xiaomeng Li *Institute of Hepatobiliary Diseases of Wuhan University, Hubei Key Laboratory of Medical Technology on Transplantation, Engineering Research Center of Natural Polymer-based Medical Materials in Hubei Province, Zhongnan Hospital of Wuhan University, Transplant Center of Wuhan University, Wuhan, 430071, China.
Ruixuan Wang *Institute of Hepatobiliary Diseases of Wuhan University, Hubei Key Laboratory of Medical Technology on Transplantation, Engineering Research Center of Natural Polymer-based Medical Materials in Hubei Province, Zhongnan Hospital of Wuhan University, Transplant Center of Wuhan University, Wuhan, 430071, China.
Donglin YangInstitute of Hepatobiliary Diseases of Wuhan University, Hubei Key Laboratory of Medical Technology on Transplantation, Engineering Research Center of Natural Polymer-based Medical Materials in Hubei Province, Zhongnan Hospital of Wuhan University, Transplant Center of Wuhan University, Wuhan, 430071, China.
Qifa YeInstitute of Hepatobiliary Diseases of Wuhan University, Hubei Key Laboratory of Medical Technology on Transplantation, Engineering Research Center of Natural Polymer-based Medical Materials in Hubei Province, Zhongnan Hospital of Wuhan University, Transplant Center of Wuhan University, Wuhan, 430071, China. yqf_china@163.com.
Zibiao ZhongInstitute of Hepatobiliary Diseases of Wuhan University, Hubei Key Laboratory of Medical Technology on Transplantation, Engineering Research Center of Natural Polymer-based Medical Materials in Hubei Province, Zhongnan Hospital of Wuhan University, Transplant Center of Wuhan University, Wuhan, 430071, China. hizzb@whu.edu.cn.

Funding

National Natural Science Foundation of China 82370758National Natural Science Foundation of China 82470685
6 · The paper itself

Abstract

Lysophosphatidic acid receptor 3 (LPA₃), a critical member of the G protein-coupled receptor (GPCR) family, plays a central role in maintaining physiological homeostasis and regulating pathological processes by modulating multiple key signaling pathways. Upon activation, LPA₃ triggers several downstream cascades, including Gαq/11, Gαi/o, and Gα12/13, thereby regulating cellular proliferation, survival, migration, inflammatory responses, and metabolic balance. LPA₃ is widely expressed in adipose tissue, the reproductive system, and the nervous system, where it exhibits tissue-specific functions. Recent studies have revealed that aberrant LPA₃ signaling is closely associated with tumorigenesis and metastasis, obesity and insulin resistance, neuroinflammation, and liver diseases. Mechanistically, LPA₃ promotes tumor cell proliferation via the PI3K/Akt and MAPK/ERK pathways, regulates glucose and lipid metabolism through the cAMP/PKA and AMPK axes, and mediates immune and inflammatory responses via NF-κB and the NLRP3 inflammasome. These multifaceted roles indicate that LPA₃ is not only an important physiological regulator but also a potential therapeutic target and biomarker. Future development of selective antagonists, biased ligands, and tissue-targeted delivery systems may enable precision interventions for cancers, metabolic disorders, and neurological diseases. This review systematically summarizes the metabolic pathways, signaling mechanisms, and physiological functions of LPA₃ and discusses its translational potential in disease therapy.

Indexed as

Receptors, Lysophosphatidic AcidSignal TransductionAnimalsHumansMetabolic DiseasesMolecular Targeted TherapyNeoplasmsReceptors, Lysophosphatidic AcidCell migrationHypoxic responseLPA₃ receptorSignal transductionTargeted therapy

Identifiers

PMID42742769

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.