Evidence map›Paper›PMID 30504760›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2018

Hypoxia-Inducible Factor 1-α (HIF-1α) Induces Apoptosis of Human Uterosacral Ligament Fibroblasts Through the Death Receptor and Mitochondrial Pathways.

Xinrui Zhao, Lidong Liu, Rui Li, Xuan Wei, Wenqing Luan, Peishu Liu, Jing Zhao

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 9% of its field
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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.

  1. Interaction of HIF-1a with various cell death pathways in tumor immune microenvironment (TIME).Apoptosis : an international journal on programmed cell death · 2026
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  5. Cancer management and research · 2026
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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

7 authors at 1 institution in 1 country.

Xinrui ZhaoDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, Shandong, China (mainland).
Lidong LiuDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, Shandong, China (mainland).
Rui LiDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, Shandong, China (mainland).
Xuan WeiDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, Shandong, China (mainland).
Wenqing LuanDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, Shandong, China (mainland).
Peishu LiuDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University , Jinan, Shandong, China (mainland).
Jing ZhaoDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, Shandong, China (mainland).
Qilu Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Hypoxia induces cell apoptosis in the uterosacral ligaments of patients with pelvic organ prolapse by upregulation of hypoxia-inducible factor-1α (HIF-1α). This study aimed to investigate the effects of HIF-1α on human uterosacral ligament fibroblasts (hUSLFs) following treatment with the chemical inducer of hypoxia, cobalt chloride (CoCl2), and to explore the underlying mechanisms. MATERIAL AND METHODS Ten women who underwent hysterectomy for benign disease provided uterosacral ligament tissue for cell extraction. Following CoCl₂ treatment, cell viability of isolated and cultured hUSLFs was evaluated by the MTT assay. JC-1 fluorescence mitochondrial imaging was used to study the change in mitochondrial membrane potential. Cell apoptosis and expression of apoptosis-associated proteins and collagen type I alpha 1 (COL1A1) were measured by flow cytometry, TUNEL and Western blot, respectively. RESULTS Hypoxia increased the expression of HIF-1a and increased cell apoptosis, decreased cell viability and expression levels of COL1A1. The JC-1 assay showed that the mitochondrial membrane potential was reduced and caspase-8, and -9 inhibitors partly reduced hUSLF apoptosis. HIF-1α treatment downregulated the expression of cellular FLICE inhibitory protein (c-FLIP), decoy receptor 2 (DcR2), and the ratio of Bcl-2 to Bax, and upregulated the expression tumor necrosis factor related apoptosis-inducing ligand (TRAIL), death receptor 5 (DR5) or TRAIL-R2, Fas, Bcl-2 interacting protein 3 (BNIP3), and cytochrome C, and increased the activation of caspase-3, caspase-8, and caspase-9, all of which were reversed by knockdown of HIF-1α. CONCLUSIONS HIF-1α significantly induced apoptosis of hUSLFs through both the cell death receptor and the mitochondrial-associated apoptosis pathways.

Indexed as

AdultApoptosisApoptosis Regulatory ProteinsCell HypoxiaCell SurvivalChinaCobaltCollagen Type ICollagen Type I, alpha 1 ChainFemaleFibroblastsHumansHypoxiaHypoxia-Inducible Factor 1, alpha SubunitLigamentsMembrane Potential, MitochondrialApoptosis Regulatory ProteinsCobaltcobaltous chlorideCOL1A1 protein, humanCollagen Type ICollagen Type I, alpha 1 ChainHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitReceptors, Death Domain

Identifiers

PMID30504760
PMCPMC6289032
OpenAlexW2903501323

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.