Evidence map›Paper›PMID 38775007›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024

The Spermine Oxidase/Spermine Axis Coordinates ATG5-Mediated Autophagy to Orchestrate Renal Senescence and Fibrosis.

Dan Luo, Xiaohui Lu, Hongyu Li, Yi Li, Yating Wang, Simin Jiang, Guanglan Li, Yiping Xu, Kefei Wu, Xianrui Dou and 4 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. 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

14 authors.

Dan LuoDepartment of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, NHC Key Laboratory of Clinical Nephrology, Guangdong Provincial Key Laboratory of Nephrology, Guangzhou, Guangdong, 510080, China.
Xiaohui LuDepartment of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, NHC Key Laboratory of Clinical Nephrology, Guangdong Provincial Key Laboratory of Nephrology, Guangzhou, Guangdong, 510080, China.
Hongyu LiDepartment of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, NHC Key Laboratory of Clinical Nephrology, Guangdong Provincial Key Laboratory of Nephrology, Guangzhou, Guangdong, 510080, China.
Yi LiDepartment of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, NHC Key Laboratory of Clinical Nephrology, Guangdong Provincial Key Laboratory of Nephrology, Guangzhou, Guangdong, 510080, China.
Yating WangDepartment of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, NHC Key Laboratory of Clinical Nephrology, Guangdong Provincial Key Laboratory of Nephrology, Guangzhou, Guangdong, 510080, China.
Simin JiangDepartment of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, NHC Key Laboratory of Clinical Nephrology, Guangdong Provincial Key Laboratory of Nephrology, Guangzhou, Guangdong, 510080, China.
Guanglan LiDepartment of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, NHC Key Laboratory of Clinical Nephrology, Guangdong Provincial Key Laboratory of Nephrology, Guangzhou, Guangdong, 510080, China.
Yiping XuDepartment of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, NHC Key Laboratory of Clinical Nephrology, Guangdong Provincial Key Laboratory of Nephrology, Guangzhou, Guangdong, 510080, China.
Kefei WuDepartment of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, NHC Key Laboratory of Clinical Nephrology, Guangdong Provincial Key Laboratory of Nephrology, Guangzhou, Guangdong, 510080, China.
Xianrui DouDepartment of Nephrology, Shunde Hospital, Southern Medical University (The First People's Hospital of Shunde), Foshan, Guangdong, 528308, China.
Qinghua LiuDepartment of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, NHC Key Laboratory of Clinical Nephrology, Guangdong Provincial Key Laboratory of Nephrology, Guangzhou, Guangdong, 510080, China.
Wei ChenDepartment of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, NHC Key Laboratory of Clinical Nephrology, Guangdong Provincial Key Laboratory of Nephrology, Guangzhou, Guangdong, 510080, China.
Yi ZhouDepartment of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, NHC Key Laboratory of Clinical Nephrology, Guangdong Provincial Key Laboratory of Nephrology, Guangzhou, Guangdong, 510080, China.
Haiping MaoDepartment of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, NHC Key Laboratory of Clinical Nephrology, Guangdong Provincial Key Laboratory of Nephrology, Guangzhou, Guangdong, 510080, China.ORCID 0000-0002-3608-3851

Funding

Guangdong Provincial Key Laboratory of Nephrology 2020B1212060028Guangdong Provincial Program of Science and Technology 2017A050503003National Natural Science Foundation of China 81870464National Natural Science Foundation of China 82000640National Natural Science Foundation of China 82070698National Natural Science Foundation of China 82270716NHC Key Laboratory of Clinical Nephrology (Sun Yat-Sen University)
6 · The paper itself

Abstract

Decreased plasma spermine levels are associated with kidney dysfunction. However, the role of spermine in kidney disease remains largely unknown. Herein, it is demonstrated that spermine oxidase (SMOX), a key enzyme governing polyamine metabolism, is predominantly induced in tubular epithelium of human and mouse fibrotic kidneys, alongside a reduction in renal spermine content in mice. Moreover, renal SMOX expression is positively correlated with kidney fibrosis and function decline in patients with chronic kidney disease. Importantly, supplementation with exogenous spermine or genetically deficient SMOX markedly improves autophagy, reduces senescence, and attenuates fibrosis in mouse kidneys. Further, downregulation of ATG5, a critical component of autophagy, in tubular epithelial cells enhances SMOX expression and reduces spermine in TGF-β1-induced fibrogenesis in vitro and kidney fibrosis in vivo. Mechanically, ATG5 readily interacts with SMOX under physiological conditions and in TGF-β1-induced fibrogenic responses to preserve cellular spermine levels. Collectively, the findings suggest SMOX/spermine axis is a potential novel therapy to antagonize renal fibrosis, possibly by coordinating autophagy and suppressing senescence.

Indexed as

AutophagyAutophagy-Related Protein 5FibrosisKidneyOxidoreductases Acting on CH-NH Group DonorsPolyamine OxidaseSpermineAnimalsCellular SenescenceDisease Models, AnimalHumansMaleMiceMice, Inbred C57BLAutophagy-Related Protein 5Oxidoreductases Acting on CH-NH Group DonorsPolyamine OxidaseSpermineautophagycell senescencerenal fibrosisSMOXspermine

Identifiers

PMID38775007
PMCPMC11304251

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.