Evidence map›Paper›PMID 29483398›Full record

ReviewChinese medical journal2018

Research Progress on the Relationship between Coronary Artery Calcification and Chronic Renal Failure.

Jun Lai, Gael Akindavyi, Qiang Fu, Zhi-Liang Li, Hui-Min Wang, Li-Hua Wen

Open access · goldAbstract readReview
In one paragraph

Review in Chinese medical journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 28% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  4. Review
  5. Article
  6. Article
  7. Observational
  8. Article
  9. Review
  10. [Zhenwu Decoction delays ventricular hypertrophy in rats with uremic cardiomyopathy].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2019
    Article
  11. Review
  12. Article
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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

6 authors at 2 institutions in 1 country.

Jun LaiDepartment of Cardiology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510280, China.
Gael AkindavyiDepartment of Cardiology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510280, China.
Qiang FuDepartment of Cardiology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510280, China.
Zhi-Liang LiDepartment of Cardiology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510280, China.
Hui-Min WangDepartment of Cardiology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510280, China.
Li-Hua WenDepartment of Cardiology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510280, China.
Southern Medical University · CNZhujiang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveCoronary artery calcification (CAC) is thought to be a controlled metabolic process that is very similar to the formation of new bone. In patients with chronic renal failure (CRF), CAC is very common, and CAC severity correlates with the deterioration of renal function. We summarized the current understanding and emerging findings of the relationship between CAC and CRF. DATA SOURCES: All studies were identified by systematically searching PubMed, Embase, and CNKI databases for the terms "coronary calcification", "chronic renal failure", "vascular smooth muscle cell", and their synonyms until September 2017. STUDY SELECTION: We examined the titles and abstracts of all studies that met our search strategy thoroughly. The full text of relevant studies was evaluated. Reference lists of retrieved articles were also scrutinized for the additional relevant studies.

resultsCRF can accelerate CAC progression. CRF increases the expression of pro-inflammatory factors, electrolyte imbalance (e.g., of calcium, phosphorus), parathyroid hormone, and uremic toxins and their ability to promote calcification. These factors, through the relevant signaling pathways, trigger vascular smooth muscle cells to transform into osteoblast-like cells while inhibiting the reduction of vascular calcification factors, thus inducing further CAC.

conclusionsCoronary heart disease in patients with CRF is due to multiple factors. Understanding the mechanism of CAC can help interventionists to protect the myocardium and reduce the prevalence of coronary heart disease and mortality.

Indexed as

Coronary Artery DiseaseCoronary RestenosisCoronary VesselsFemaleHumansKidney Failure, ChronicMaleMuscle, Smooth, VascularMyocytes, Smooth MuscleChronic Renal FailureCoronary CalcificationVascular Smooth Muscle Cell

Identifiers

PMID29483398
PMCPMC5850680
OpenAlexW2791036985

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.