Evidence map›Paper›PMID 38844470›Full record

ArticleCell death & disease2024

HOXD10 attenuates renal fibrosis by inhibiting NOX4-induced ferroptosis.

Xin Li, Tian-Kui Ma, Pu Wang, Hang Shi, Sang Hai, Yu Qin, Yun Zou, Wan-Ting Zhu, Hui-Min Li, Yan-Nong Li and 5 more

Abstract read
In one paragraph

Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed.

  1. Review
  2. Ferroptosis in kidney disease.Nature reviews. Nephrology · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. The Hypoglycemic Activity ofGels (Basel, Switzerland) · 2025
    Article
  19. Article
  20. 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

15 authors.

Xin Li *Nephrology Department, Fourth Hospital of China Medical University, Shenyang, China.
Tian-Kui Ma *Biological Therapy Department, First Hospital of China Medical University, Shenyang, China.
Pu WangGeneral Practice Department, Fourth Hospital of China Medical University, Shenyang, China.
Hang ShiIntensive Care Unit Department, Sun Yat-sen Memorial Hospital, Guangzhou, China.
Sang HaiNephrology Department, Fourth Hospital of China Medical University, Shenyang, China.
Yu QinNephrology Department, Fourth Hospital of China Medical University, Shenyang, China.
Yun ZouNephrology Department, Fourth Hospital of China Medical University, Shenyang, China.
Wan-Ting ZhuNephrology Department, Fourth Hospital of China Medical University, Shenyang, China.
Hui-Min LiNephrology Department, Fourth Hospital of China Medical University, Shenyang, China.
Yan-Nong LiNephrology Department, Fourth Hospital of China Medical University, Shenyang, China.
Li YinNephrology Department, Fourth Hospital of China Medical University, Shenyang, China.
Yan-Yan XuNephrology Department, Fourth Hospital of China Medical University, Shenyang, China.
Qi YangNephrology Department, Fourth Hospital of China Medical University, Shenyang, China.
Shuang ZhangNephrology Department, Fourth Hospital of China Medical University, Shenyang, China.
Hong DingNephrology Department, Fourth Hospital of China Medical University, Shenyang, China. dinghong9209@126.com.ORCID 0000-0002-2388-721X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In chronic kidney disease (CKD), renal fibrosis is an unavoidable result of various manifestations. However, its pathogenesis is not yet fully understood. Here, we revealed the novel role of Homeobox D10 (HOXD10) in CKD-related fibrosis. HOXD10 expression was downregulated in CKD-related in vitro and in vivo fibrosis models. UUO model mice were administered adeno-associated virus (AAV) containing HOXD10, and HOXD10 overexpression plasmids were introduced into human proximal tubular epithelial cells induced by TGF-β1. The levels of iron, reactive oxygen species (ROS), lipid ROS, the oxidized glutathione/total glutathione (GSSG/GSH) ratio, malonaldehyde (MDA), and superoxide dismutase (SOD) were determined using respective assay kits. Treatment with AAV-HOXD10 significantly attenuated fibrosis and renal dysfunction in UUO model mice by inhibiting NOX4 transcription, ferroptosis pathway activation, and oxidative stress. High levels of NOX4 transcription, ferroptosis pathway activation and profibrotic gene expression induced by TGF-β1/erastin (a ferroptosis agonist) were abrogated by HOXD10 overexpression in HK-2 cells. Moreover, bisulfite sequencing PCR result determined that HOXD10 showed a hypermethylated level in TGF-β1-treated HK-2 cells. The binding of HOXD10 to the NOX4 promoter was confirmed by chromatin immunoprecipitation (ChIP) analysis and dual-luciferase reporter assays. Targeting HOXD10 may represent an innovative therapeutic strategy for fibrosis treatment in CKD.

Indexed as

FerroptosisFibrosisHomeodomain ProteinsNADPH Oxidase 4Renal Insufficiency, ChronicAnimalsCell LineDisease Models, AnimalHumansKidneyMaleMiceMice, Inbred C57BLOxidative StressReactive Oxygen SpeciesTranscription FactorsHomeodomain ProteinsNADPH Oxidase 4NOX4 protein, humanNox4 protein, mouseReactive Oxygen SpeciesTranscription FactorsTransforming Growth Factor beta1

Identifiers

PMID38844470
PMCPMC11156659

What Socratic 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 Socratic graph.