Evidence map›Paper›PMID 39138590›Full record

ArticleRedox report : communications in free radical research2024

Sigma-1 receptor exerts protective effects on ameliorating nephrolithiasis by modulating endoplasmic reticulum-mitochondrion association and inhibiting endoplasmic reticulum stress-induced apoptosis in renal tubular epithelial cells.

Hu Ke, Xiaozhe Su, Caitao Dong, Ziqi He, Qianlin Song, Chao Song, Jiawei Zhou, Wenbiao Liao, Chuan Wang, Sixing Yang and 1 more

Abstract read
In one paragraph

Article in Redox report : communications in free radical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Extracts ofPharmaceuticals (Basel, Switzerland) · 2026
    Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Total flavonoids ofFrontiers in pharmacology · 2026
    Article
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  10. Article
  11. Article
  12. Review
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

11 authors.

Hu KeUrology Department, Renmin Hospital of Wuhan University, Wuhan, People's Republic of China.
Xiaozhe SuUrology Department, Renmin Hospital of Wuhan University, Wuhan, People's Republic of China.
Caitao DongUrology Department, Renmin Hospital of Wuhan University, Wuhan, People's Republic of China.
Ziqi HeUrology Department, Renmin Hospital of Wuhan University, Wuhan, People's Republic of China.
Qianlin SongUrology Department, Renmin Hospital of Wuhan University, Wuhan, People's Republic of China.
Chao SongUrology Department, Renmin Hospital of Wuhan University, Wuhan, People's Republic of China.
Jiawei ZhouUrology Department, Renmin Hospital of Wuhan University, Wuhan, People's Republic of China.
Wenbiao LiaoUrology Department, Renmin Hospital of Wuhan University, Wuhan, People's Republic of China.
Chuan WangUrology Department, Renmin Hospital of Wuhan University, Wuhan, People's Republic of China.
Sixing YangUrology Department, Renmin Hospital of Wuhan University, Wuhan, People's Republic of China.
Yunhe XiongUrology Department, Renmin Hospital of Wuhan University, Wuhan, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxalate-induced damage to renal tubular epithelial cells (RTECs) is an essential factor in the incident kidney stone, but the specific mechanism is unclear. Recent research has pinpointed interacting areas within the endoplasmic reticulum and mitochondria, called mitochondria-associated membranes (MAMs). These studies have linked endoplasmic reticulum stress (ERS) and oxidative imbalance to kidney disease development. The sigma-1 receptor (S1R), a specific protein found in MAMs, is involved in various physiological processes, but its role in oxalate-induced kidney stone formation remains unclear. In this study, we established cellular and rat models of oxalate-induced kidney stone formation to elucidate the S1R's effects against ERS and apoptosis and its mechanism in oxalate-induced RTEC injury. We found that oxalate downregulated S1R expression in RTECs and escalated oxidative stress and ERS, culminating in increased apoptosis. The S1R agonist dimemorfan up-regulated S1R expression and mitigated ERS and oxidative stress, thereby reducing apoptosis. This protective effect was mediated through S1R inhibition of the CHOP pathway. Animal experiments demonstrated that S1R's activation attenuated oxalate-induced kidney injury and alleviated kidney stone formation. This is the first study to establish the connection between S1R and kidney stones, suggesting S1R's protective role in inhibiting ERS-mediated apoptosis to ameliorate kidney stone formation.

Indexed as

ApoptosisEndoplasmic ReticulumEndoplasmic Reticulum StressEpithelial CellsKidney TubulesMitochondriaNephrolithiasisReceptors, sigmaSigma-1 ReceptorAnimalsMaleOxidative StressRatsRats, Sprague-DawleyOprs1 protein, ratReceptors, sigmaSigma-1 Receptorapoptosisdimemorfanendoplasmic reticulum stresskidney stonemitochondria-associated endoplasmic reticulum membraneoxalateoxidative stressSigmar-1 receptor

Identifiers

PMID39138590
PMCPMC11328816

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Registered trials

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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 OpenQuestion graph.