In one paragraphArticle in The Journal of experimental medicine, 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
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 registryThe 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 literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
10 authors.
Yunfeng Zhou *Guangdong Provincial Key Laboratory of Infection Immunity and Inflammation, Department of Physiology and Immunology, School of Basic Medical Sciences, International Cancer Center, Shenzhen University Medical School, Shenzhen University, Shenzhen, China.ORCID 0000-0001-8747-0678 Ying Zhang *Guangdong Provincial Key Laboratory of Infection Immunity and Inflammation, Department of Physiology and Immunology, School of Basic Medical Sciences, International Cancer Center, Shenzhen University Medical School, Shenzhen University, Shenzhen, China.ORCID 0009-0003-5146-7380 Miao ZhuGuangdong Provincial Key Laboratory of Infection Immunity and Inflammation, Department of Physiology and Immunology, School of Basic Medical Sciences, International Cancer Center, Shenzhen University Medical School, Shenzhen University, Shenzhen, China.ORCID 0009-0008-2712-0762 Chenghui LiaoGuangdong Provincial Key Laboratory of Infection Immunity and Inflammation, Department of Physiology and Immunology, School of Basic Medical Sciences, International Cancer Center, Shenzhen University Medical School, Shenzhen University, Shenzhen, China.ORCID 0009-0008-8694-0023 Weie LiGuangdong Provincial Key Laboratory of Infection Immunity and Inflammation, Department of Physiology and Immunology, School of Basic Medical Sciences, International Cancer Center, Shenzhen University Medical School, Shenzhen University, Shenzhen, China.ORCID 0009-0000-3740-0911 Tie ChenSchool of Pharmacy, Shenzhen University Medical School, Shenzhen University , Shenzhen, China.ORCID 0009-0006-0802-2150 Yuan ChengDepartment of Nephrology, Shenzhen Second People's Hospital, First Affiliated Hospital of Shenzhen University, Shenzhen, China.ORCID 0000-0003-2677-0698 Liang YeGuangdong Provincial Key Laboratory of Infection Immunity and Inflammation, Department of Physiology and Immunology, School of Basic Medical Sciences, International Cancer Center, Shenzhen University Medical School, Shenzhen University, Shenzhen, China.ORCID 0000-0002-6735-0836 Funding
Albert-Ludwigs-Universität Freiburg, UniversitätsbibliothekNational Natural Science Foundation of China 32170937National Natural Science Foundation of China 82270759National Natural Science Foundation of China 82572024Pearl River Talent Project of Guangdong Province 2021QN02Y426Shenzhen Medical Research Fund A2303015Shenzhen Peacock Plan Project 827000655Shenzhen Science and Technology program JCYJ20210324095005015Shenzhen Science and Technology program JCYJ20250604181042019
6 · The paper itselfAbstract
Renal fibrosis is a critical step in chronic kidney disease (CKD) progression, but fibrosis induction is still not understood well. We found that IFN-λ is a profibrotic factor that is upregulated in fibrotic human and mouse kidneys. IFN-λ receptor deficiency ameliorated renal fibrosis in mice while exogenous IFN-λ exacerbated disease, establishing a detrimental role of IFN-λ signaling in renal fibrosis. Mechanistically, we found that IFN-λ promotes fibrosis by preferentially acting on renal fibroblasts, inducing their activation and migration through ERK/JNK-dependent synthesis of TGF-β and activation of the TGF-β-SMAD2/3 signaling pathway. Renal tubular epithelial cell (TEC)-derived IFN-λ induced by RIG-I/MAVS signaling emerged as a critical driver of renal fibroblast activation and fibrogenesis. Importantly, neutralizing antibodies against IFN-λ strongly attenuated renal fibrosis in mice. Thus, the renal TEC-IFN-λ-fibroblast axis is a previously unrecognized pathway of renal fibrosis induction that represents an attractive novel target for mitigating CKD progression.
Indexed as
Epithelial CellsFibroblastsInterferonsInterleukinsKidneyRenal Insufficiency, ChronicAnimalsFibrosisHumansInterferon LambdaMaleMiceMice, Inbred C57BLMice, KnockoutReceptors, InterferonSignal TransductionInterferon Lambdainterferon-lambda protein, mouseInterferonsInterleukinsReceptors, InterferonTransforming Growth Factor beta
Identifiers
PMID42405949
PMCPMC13335421
What Socratic holds
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LicenceCC BY
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