Evidence map›Paper›PMID 41909672›Full record

ArticleFrontiers in immunology2026

Selective JAK2 inhibition by TG101209 reprograms macrophage polarization and alleviates acute lung injury.

Jinxian Ye, Youguang Pan, Canchao Jia, Sijia Liu, Xiang Li, Lixin Zhao, Jiandong Zhang, Xiying Chen, Bingyu Zheng, Zhiyu Chen and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article 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.

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0cells of the map it votes in
0citing papers in PubMed
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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

15 authors.

Jinxian Ye *The Fifth Affiliated Hospital, Key Laboratory of Molecular Target and Clinical Pharmacology, NMPA, and the State Key Laboratory of Respiratory Disease, The School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou, China.
Youguang Pan *Department of Thoracic Surgery, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China.
Canchao Jia *The Fifth Affiliated Hospital, Key Laboratory of Molecular Target and Clinical Pharmacology, NMPA, and the State Key Laboratory of Respiratory Disease, The School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou, China.
Sijia LiuThe Fifth Affiliated Hospital, Key Laboratory of Molecular Target and Clinical Pharmacology, NMPA, and the State Key Laboratory of Respiratory Disease, The School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou, China.
Xiang LiThe Fifth Affiliated Hospital, Key Laboratory of Molecular Target and Clinical Pharmacology, NMPA, and the State Key Laboratory of Respiratory Disease, The School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou, China.
Lixin ZhaoThe Fifth Affiliated Hospital, Key Laboratory of Molecular Target and Clinical Pharmacology, NMPA, and the State Key Laboratory of Respiratory Disease, The School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou, China.
Jiandong ZhangThe Fifth Affiliated Hospital, Key Laboratory of Molecular Target and Clinical Pharmacology, NMPA, and the State Key Laboratory of Respiratory Disease, The School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou, China.
Xiying ChenThe Fifth Affiliated Hospital, Key Laboratory of Molecular Target and Clinical Pharmacology, NMPA, and the State Key Laboratory of Respiratory Disease, The School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou, China.
Bingyu ZhengThe Fifth Affiliated Hospital, Key Laboratory of Molecular Target and Clinical Pharmacology, NMPA, and the State Key Laboratory of Respiratory Disease, The School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou, China.
Zhiyu ChenThe Fifth Affiliated Hospital, Key Laboratory of Molecular Target and Clinical Pharmacology, NMPA, and the State Key Laboratory of Respiratory Disease, The School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou, China.
Juan YangState Key Laboratory of New Targets Discovery and Drug Development for Major Diseases, Gannan Innovation and Translational Medicine Research Institute, Gannan Medical University, Ganzhou, China.
Zhongxiao LinThe Fifth Affiliated Hospital, Key Laboratory of Molecular Target and Clinical Pharmacology, NMPA, and the State Key Laboratory of Respiratory Disease, The School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou, China.
Ao ShenThe Fifth Affiliated Hospital, Key Laboratory of Molecular Target and Clinical Pharmacology, NMPA, and the State Key Laboratory of Respiratory Disease, The School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou, China.
Xin YangThe Fifth Affiliated Hospital, Key Laboratory of Molecular Target and Clinical Pharmacology, NMPA, and the State Key Laboratory of Respiratory Disease, The School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou, China.
Lu LiangThe Fifth Affiliated Hospital, Key Laboratory of Molecular Target and Clinical Pharmacology, NMPA, and the State Key Laboratory of Respiratory Disease, The School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Acute lung injury (ALI) represents a critical respiratory syndrome involving extensive alveolar injury and uncontrolled inflammation, yet it continues to exhibit high mortality rates in the absence of effective treatments. Here we evaluate TG101209, a selective Janus kinase 2 (JAK2) inhibitor, as a modulator of macrophage polarization and a candidate intervention for ALI. Methods: This study employed both in vivo and in vitro models to investigate the protective effects of TG101209 against ALI. Using lipopolysaccharide (LPS)-induced ALI mice and RAW264.7 inflammatory injury models, the JAK2/STAT3 signaling axis was validated by western blotting and immunofluorescence. Results: TG101209 alleviated pulmonary inflammation, improved lung function, inhibited M1 polarization, and promoted M2 polarization. Specifically, TG101209 downregulated CD80 and iNOS while upregulating CD163 and Arg1 at both mRNA and protein levels. TG101209 treatment markedly decreased the phosphorylation levels of JAK2 and STAT3 at Ser727 and Tyr705. Conclusion: TG101209 promotes macrophage polarization toward the M2 phenotype by blocking JAK2/STAT3 activation, indicating its therapeutic value in ALI.

Indexed as

Acute Lung InjuryJanus Kinase 2Macrophage ActivationMacrophagesSulfonamidesAnimalsDisease Models, AnimalLipopolysaccharidesMaleMiceMice, Inbred C57BLRAW 264.7 CellsSignal TransductionSTAT3 Transcription FactorJak2 protein, mouseJanus Kinase 2LipopolysaccharidesStat3 protein, mouseSTAT3 Transcription FactorSulfonamidesacute lung injury (ALI)inflammationJAK2/STAT3 signalingmacrophage polarizationTG101209

Identifiers

PMID41909672
PMCPMC13021449

What Socratic 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 Socratic graph.