Evidence map›Paper›PMID 41294012›Full record

ArticleJournal of cellular and molecular medicine2025

Silencing of Cholesterol 25-Hydroxylase Attenuates Lipopolysaccharide-Induced Cardiomyocyte Damage In Vitro.

Yi-Jiao Men, Hong-Bo Cheng, Yan-Ling Dong, Yu Gong, Ya-Qing An, Ying-Li Jin, Shu-Na Hao, Yu Ma, Ying-Ping Tian

Abstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2025. 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

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

1 citing paper in PubMed.

  1. 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

9 authors.

Yi-Jiao MenDepartment of Emergency, The Second Hospital of Hebei Medical University, Shijiazhuang, China.ORCID 0009-0006-3618-7307
Hong-Bo ChengDepartment of Emergency, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Yan-Ling DongDepartment of Emergency, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Yu GongDepartment of Emergency, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Ya-Qing AnDepartment of Emergency, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Ying-Li JinDepartment of Emergency, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Shu-Na HaoDepartment of Emergency, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Yu MaDepartment of Emergency, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Ying-Ping TianDepartment of Emergency, The Second Hospital of Hebei Medical University, Shijiazhuang, China.

Funding

Peking Union Medical Foundation-Ruiyi Emergency Medical Research Fund 22222012010Scientific Research Fund Project of the Hebei Provincial Health and Family Planning Commission 20211690
6 · The paper itself

Abstract

The underlying mechanisms of sepsis-induced myocardial dysfunction (SIMD) remain elusive, and no targeted therapies currently exist. This study aimed to explore the expression features and functional effects of cholesterol 25-hydroxylase (CH25H) in SIMD in vitro. CH25H was identified as an upregulated gene related to SIMD through bioinformatics analysis. Its upregulation was validated in the myocardial tissue of SIMD mice as well as in lipopolysaccharide (LPS)-induced primary cardiomyocytes and AC16 cells. CH25H overexpression elevated 25-hydroxycholesterol levels and aggravated oxidative stress, mitochondrial dysfunction, apoptosis, and NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome and NF-κB pathway activation in AC16 cells. The effect of CH25H overexpression was similar to that induced by LPS treatment. Conversely, silencing CH25H attenuated these LPS-induced injuries. Furthermore, CH25H overexpression exacerbated oxidative stress, mitochondrial dysfunction, and apoptosis in LPS-stimulated AC16 cells, and these effects of CH25H overexpression can be counteracted by the NLRP3 inhibitor. In conclusion, CH25H may promote LPS-induced cardiomyocyte injury through NLRP3/NF-κB pathway activation.

Indexed as

Gene SilencingLipopolysaccharidesMyocytes, CardiacAnimalsApoptosisHydroxycholesterolsInflammasomesMaleMiceMitochondriaNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinOxidative StressSignal TransductionSteroid Hydroxylases25-hydroxycholesterolcholesterol 25-hydroxylaseHydroxycholesterolsInflammasomesLipopolysaccharidesNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinSteroid HydroxylasesapoptosisCH25Hmitochondrial dysfunctionoxidative stresssepsis‐induced myocardial dysfunction

Identifiers

PMID41294012
PMCPMC12648292

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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.