Evidence map›Paper›PMID 38107584›Full record

ArticlePeerJ2023

Involvement of plasminogen activator inhibitor-1 in p300/p53-mediated age-related atrial fibrosis.

Yingyu Lai, Jintao He, Xiaoyan Gao, Dewei Peng, Huishan Zhou, Yuwen Xu, Xueshan Luo, Hui Yang, Mengzhen Zhang, Chunyu Deng and 4 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PeerJ, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.7field-weighted citation impact, top 26% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. Review
  3. 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

14 authors at 5 institutions in 1 country.

Yingyu Lai *Medical Research Institute, Guangdong Provincial Key Laboratory of Clinical Pharmacology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, China.
Jintao He *School of Medicine, South China University of Technology, Guangzhou, Guangdong, China.
Xiaoyan GaoMedical Research Institute, Guangdong Provincial Key Laboratory of Clinical Pharmacology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, China.
Dewei PengMedical Research Institute, Guangdong Provincial Key Laboratory of Clinical Pharmacology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, China.
Huishan ZhouMedical Research Institute, Guangdong Provincial Key Laboratory of Clinical Pharmacology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, China.
Yuwen XuMedical Research Institute, Guangdong Provincial Key Laboratory of Clinical Pharmacology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, China.
Xueshan LuoMedical Research Institute, Guangdong Provincial Key Laboratory of Clinical Pharmacology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, China.
Hui YangMedical Research Institute, Guangdong Provincial Key Laboratory of Clinical Pharmacology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, China.
Mengzhen ZhangMedical Research Institute, Guangdong Provincial Key Laboratory of Clinical Pharmacology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, China.
Chunyu DengMedical Research Institute, Guangdong Provincial Key Laboratory of Clinical Pharmacology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, China.
Shulin WuMedical Research Institute, Guangdong Provincial Key Laboratory of Clinical Pharmacology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, China.
Yumei XueMedical Research Institute, Guangdong Provincial Key Laboratory of Clinical Pharmacology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, China.
Feng ZhouDepartment of Neurology, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, Guangdong, China.
Fang RaoMedical Research Institute, Guangdong Provincial Key Laboratory of Clinical Pharmacology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, China.
Guangdong Provincial People's Hospital · CNSouthern Medical University · CNGuangdong Academy of Medical Sciences · CNSouth China University of Technology · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Plasminogen activator inhibitor-1 (PAI-1), a key regulator of the fibrinolytic system, is also intimately involved in the fibrosis. Although PAI-1 may be involved in the occurrence of atrial fibrillation (AF) and thrombosis in the elderly, but whether it participated in aging-related atrial fibrosis and the detailed mechanism is still unclear. We compared the transcriptomics data of young (passage 4) versus senescent (passage 14) human atrial fibroblasts and found that PAI-1 was closely related to aging-related fibrosis. Aged mice and senescent human and mouse atrial fibroblasts underwent electrophysiological and biochemical studies. We found that p300, p53, and PAI-1 protein expressions were increased in the atrial tissue of aged mice and senescent human and mouse atrial fibroblasts. Curcumin or C646 (p300 inhibitor), or p300 knockdown inhibited the expression of PAI-1 contributing to reduced atrial fibroblasts senescence, atrial fibrosis, and the AF inducibility. Furthermore, p53 knockdown decreased the protein expression of PAI-1 and p21 in senescent human and mouse atrial fibroblasts. Our results suggest that p300/p53/PAI-1 signaling pathway participates in the mechanism of atrial fibrosis induced by aging, which provides new sights into the treatment of elderly AF.

Indexed as

Plasminogen Activator Inhibitor 1Tumor Suppressor Protein p53AgingAnimalsFibrosisHumansMicePlasminogen Activator Inhibitor 1Tumor Suppressor Protein p53Age-related atrial fibrosisAtrial fibrillationBioinformatics analysisFibrinolytic systemp300p53Plasminogen activator inhibitor-1SenescenceThrombosis

Identifiers

PMID38107584
PMCPMC10722982
OpenAlexW4389623209

What OpenQuestion holds

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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.