Evidence map›Paper›PMID 28601780›Full record

ArticleRedox biology2017

SIRT1 inhibition causes oxidative stress and inflammation in patients with coronary artery disease.

Shih-Hung Chan, Ching-Hsia Hung, Jhih-Yuan Shih, Pei-Ming Chu, Yung-Hsin Cheng, Huei-Chen Lin, Kun-Ling Tsai

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

Article in Redox biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 2 pooled it
3.4field-weighted citation impact, top 7% 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

45 citing papers in PubMed, 2 syntheses or guidelines pooled it, 86 citations in OpenAlex.

  1. Pooled it
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  13. NADCell communication and signaling : CCS · 2024
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  19. Evaluation of Rosuvastatin Therapy onCurrent therapeutic research, clinical and experimental · 2023
    Article
  20. The sirtuin family in health and disease.Signal transduction and targeted therapy · 2022
    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

7 authors at 5 institutions in 1 country.

Shih-Hung ChanDepartment of Internal Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Ching-Hsia HungDepartment of Physical Therapy, College of Medicine, National Cheng Kung University, Tainan, Taiwan; Institute of Allied Health Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Jhih-Yuan ShihDepartment of Internal Medicine, Chi-Mei Hospital, Tainan, Taiwan.
Pei-Ming ChuDepartment of Anatomy, School of Medicine, China Medical University, Taichung, Taiwan.
Yung-Hsin ChengDepartment of Education and Research, Taipei City Hospital, Taipei, Taiwan.
Huei-Chen LinInstitute of Allied Health Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan; Department of Physical Therapy, Shu-Zen Junior College of Medicine and Management, Taiwan.
Kun-Ling TsaiDepartment of Physical Therapy, College of Medicine, National Cheng Kung University, Tainan, Taiwan. Electronic address: kunlingtsai@mail.ncku.edu.tw.
National Cheng Kung University · TWChi Mei Medical Center · TWChina Medical University · TWNational Cheng Kung University Hospital · TWTaipei City Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coronary artery disease (CAD) is the primary critical cardiovascular event. Endothelial cell and monocyte dysfunction with subsequent extravagant inflammation are the main causes of vessel damage in CAD. Thus, strategies that repress cell death and manage unsuitable pro-inflammatory responses in CAD are potential therapeutic strategies for improving the clinical prognosis of patients with CAD. SIRT1 (Sirtuin 1) plays an important role in regulating cellular physiological processes. SIRT1 is also thought to protect the cardiovascular system by means of its antioxidant, anti-inflammation and anti-apoptosis activities. In the present study, we found that the SIRT1 expression levels were repressed and the acetylated p53 expression levels were enhanced in the monocytes of patients with CAD. LOX-1/oxidative stress was also up-regulated in the monocytes of patients with CAD, thereby increasing pro-apoptotic events and pro-inflammatory responses. We also demonstrated that monocytes from CAD patients caused endothelial adhesion molecule activation and the adherence of monocytes and endothelial cells. Our findings may explain why CAD patients remain at an increased risk of long-term recurrent ischemic events and provide new knowledge regarding the management of clinical CAD patients.

Indexed as

Oxidative StressAdultApoptosisCoronary Artery DiseaseFemaleHumansHuman Umbilical Vein Endothelial CellsMaleMiddle AgedMonocytesScavenger Receptors, Class ESirtuin 1Tumor Suppressor Protein p53OLR1 protein, humanScavenger Receptors, Class ESIRT1 protein, humanSirtuin 1Tumor Suppressor Protein p53CADLOX-1Oxidative stressSIRT1

Identifiers

PMID28601780
PMCPMC5466584
OpenAlexW2620948159

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.