Evidence map›Paper›PMID 39375532›Full record

ArticleExperimental & molecular medicine2024

Unveiling the role of transgelin as a prognostic and therapeutic target in kidney fibrosis via a proteomic approach.

Soie Kwon, Seongmin Cheon, Kyu-Hong Kim, Areum Seo, Eunjin Bae, Jae Wook Lee, Ran-Hui Cha, Jin Ho Hwang, Yong Chul Kim, Dong Ki Kim and 3 more

Abstract read
In one paragraph

Article in Experimental & molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Article
  3. The circadian clock controls hepatic stellate cell activation via a BMAL1/CK1ε/REV-ERBα/transgelin signaling pathway.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Article
  5. Article
  6. Article
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

13 authors.

Soie Kwon *Department of Internal Medicine, Chung-Ang University Hospital, Seoul, Republic of Korea.
Seongmin Cheon *School of Biological Sciences and Technology, Chonnam National University, Gwangju, Republic of Korea.
Kyu-Hong KimKidney Research Institute, Seoul National University College of Medicine, Seoul, Republic of Korea.
Areum SeoKidney Research Institute, Seoul National University College of Medicine, Seoul, Republic of Korea.
Eunjin BaeDepartment of Internal Medicine, Gyeongsang National University College of Medicine, Gyeongsang University Changwon Hospital, Gyeongsang, Republic of Korea.
Jae Wook LeeNephrology Clinic, National Cancer Center of Korea, Seoul, Republic of Korea.
Ran-Hui ChaBiomedical Research Institute, Seoul National University Hospital, Seoul, Republic of Korea.
Jin Ho HwangDepartment of Internal Medicine, Chung-Ang University Hospital, Seoul, Republic of Korea.
Yong Chul KimDepartment of Internal Medicine, Seoul National University Hospital, Seoul, Republic of Korea.
Dong Ki KimDepartment of Internal Medicine, Seoul National University Hospital, Seoul, Republic of Korea.
Yon Su KimKidney Research Institute, Seoul National University College of Medicine, Seoul, Republic of Korea.
Dohyun HanProteomics Core Facility, Biomedical Research Institute, Seoul National University Hospital, Seoul, Republic of Korea. hdh03@snu.ac.kr.ORCID 0000-0002-0841-1598
Seung-Hee YangKidney Research Institute, Seoul National University College of Medicine, Seoul, Republic of Korea. ysh5794@snu.ac.kr.

Funding

National Research Foundation of Korea (NRF) 2020R1A5A1019023National Research Foundation of Korea (NRF) 2023R1A2C2006651
6 · The paper itself

Abstract

Chronic kidney disease (CKD) progression involves tubulointerstitial fibrosis, a process characterized by excessive extracellular matrix accumulation. To identify potential biomarkers for kidney fibrosis, we performed mass spectrometry-based proteomic profiling of human kidney tubular epithelial cells and kidney tissue from a 5/6 nephrectomy rat model. Multidisciplinary analysis across kidney fibrosis models revealed 351 differentially expressed proteins associated with kidney fibrosis, and they were enriched in processes related to the extracellular matrix, kidney aging, and mitochondrial functions. Network analysis of the selected proteins revealed five crucial proteins, of which transgelin emerged as a candidate protein that interacts with known fibrosis-related proteins. Concordantly, the gene expression of transgelin in the kidney tissue from the 5/6 nephrectomy model was elevated. Transgelin expression in kidney tissue gradually increased from intermediate to advanced fibrosis stages in 5/6 Nx rats and mice with unilateral ureteral obstruction. Subsequent validation in kidney tissue and urine samples from patients with CKD confirmed the upregulation of transgelin, particularly under advanced disease stages. Moreover, we investigated whether blocking TAGLN ameliorated kidney fibrosis and reduced reactive oxygen species levels in cellular models. In conclusion, our proteomic approach identified TAGLN as a potential noninvasive biomarker and therapeutic target for CKD-associated kidney fibrosis, suggesting its role in modulating mitochondrial dysfunction and oxidative stress responses.

Indexed as

BiomarkersFibrosisMicrofilament ProteinsMuscle ProteinsProteomicsAnimalsDisease Models, AnimalHumansKidneyMaleMiceOxidative StressPrognosisProteomeRatsRenal Insufficiency, ChronicBiomarkersMicrofilament ProteinsMuscle ProteinsProteometransgelin

Identifiers

PMID39375532
PMCPMC11542076

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.