Evidence map›Paper›PMID 39283550›Full record

ArticleClinical rheumatology2024

Unraveling the proteomic landscape of fibrosis in lupus nephritis through CI-based analysis.

Fan Zhang, Ping Li, Ying Shan, Zhiwei Lai, Shuang Hou, Zibo Xiong, Zuying Xiong, Xiaoyan Huang, Fengping Zheng

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Article in Clinical rheumatology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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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

1 citing paper in PubMed.

  1. Review
4 · The record

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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

9 authors.

Fan ZhangDepartment of Nephrology, Peking University Shenzhen Hospital, Shenzhen, Guangdong Province, China.
Ping LiDepartment of Pathology, Peking University Shenzhen Hospital, Shenzhen, Guangdong Province, China.
Ying ShanClinical Research Academy, Peking University Shenzhen Hospital, Peking University, Shenzhen, Guangdong Province, China.
Zhiwei LaiDepartment of Nephrology, Peking University Shenzhen Hospital, Shenzhen, Guangdong Province, China.
Shuang HouDepartment of Nephrology, Peking University Shenzhen Hospital, Shenzhen, Guangdong Province, China.
Zibo XiongDepartment of Nephrology, Peking University Shenzhen Hospital, Shenzhen, Guangdong Province, China.
Zuying XiongDepartment of Nephrology, Peking University Shenzhen Hospital, Shenzhen, Guangdong Province, China.
Xiaoyan HuangDepartment of Nephrology, Peking University Shenzhen Hospital, Shenzhen, Guangdong Province, China. huangxiaoyan@pku.org.cn.
Fengping ZhengDepartment of Nephrology, Peking University Shenzhen Hospital, Shenzhen, Guangdong Province, China. pennycheng01@163.com.ORCID http://orcid.org/0000-0002-6065-3500

Funding

henzhen Science and Technology Innovation Commission JCYJ20200109140412476National Natural Science Foundation of China 82302042
6 · The paper itself

Abstract

introductionThe underlying mechanism by which lupus nephritis (LN) progresses to chronic kidney disease remains elusive. Fibrosis is a hallmark feature of chronic kidney disease, including LN. The chronicity index (CI) score, which incorporates glomerular sclerosis, fibrous crescents, tubular atrophy, and interstitial fibrosis, summarizes the extent of kidney tissue fibrosis.

methodIn this study, we employed label-free quantitative proteomics based on mass spectrometry to generate kidney protein profiles with varying CI scores.

resultsA total of 98 proteins exhibiting linear correlation with CI scores were initially screened out by linear model (CI linearly related proteins), and subsequently, 12 key proteins were derived based on the CI linearly related proteins using Cytohubba. LN patients were stratified into two subtypes based on CI scores and epithelial-mesenchymal transition (EMT) characteristics. These subtypes exhibited significant disparities in immune infiltration and molecular pathways. The high EMT group exhibited heightened activation of immune cells, such as memory B cells, gamma delta T cells, and resting mast cells. Gene Set Enrichment Analysis (GSEA) uncovered substantial dysregulation in critical biological processes and signaling pathways, including NF-κB, JNK, PI3K/AKT/mTOR signaling pathway, lipoprotein biosynthetic process, and endocytosis, in both subgroups.

conclusionIn conclusion, this study establishes molecular subgroups based on the CI score, providing novel insights into the molecular mechanisms governing chronicity in the kidneys of diverse LN patients. Key Points • Fibrosis is a fundamental and characteristic pathological process underlying the NIH-CI in LN. • Different EMT status presented variant clinical characteristics, immune features in LN.

Indexed as

FibrosisKidneyLupus NephritisProteomicsAdultEpithelial-Mesenchymal TransitionFemaleHumansMaleMiddle AgedRenal Insufficiency, ChronicSignal TransductionChronicity indexEpithelial-mesenchymal transitionImmune cellsLupus nephritis

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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.