Evidence map›Paper›PMID 28978867›Full record

ReviewJournal of atherosclerosis and thrombosis2018

Cysteine Protease Cathepsins in Atherosclerotic Cardiovascular Diseases.

Hongxian Wu, Qiuna Du, Qiuyan Dai, Junbo Ge, Xianwu Cheng

Abstract readReview
In one paragraph

Review in Journal of atherosclerosis and thrombosis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing 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

57 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Vascular Extracellular Matrix in Atherosclerosis.International journal of molecular sciences · 2024
    Review
  11. Article
  12. Article
  13. Advances in Cathepsin S Inhibition: Challenges and Breakthroughs in Drug Development.Pathophysiology : the official journal of the International Society for Pathophysiology · 2024
    Review
  14. Article
  15. Cathepsin K deficiency prevented stress-related thrombosis in a mouse FeClCellular and molecular life sciences : CMLS · 2024
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

5 authors.

Hongxian WuShanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University.
Qiuna DuDepartment of Nephrology, Tongji Hospital, Tongji University.
Qiuyan DaiDepartment of Cardiology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine.
Junbo GeShanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University.
Xianwu ChengDepartment of Cardiology, Yanbian University Hospital.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerotic cardiovascular disease (ASCVD) is an inflammatory disease characterized by extensive arterial wall matrix protein degradation. Cysteine protease cathepsins play a pivotal role in extracellular matrix (ECM) remodeling and have been implicated in the development and progression of atherosclerosis-based cardiovascular diseases. An imbalance in expression between cathepsins (such as cathepsins S, K, L, C) and their inhibitor cystatin C may favor proteolysis of ECM in the pathogenesis of cardiovascular disease such as atherosclerosis, aneurysm formation, restenosis, and neovascularization. New insights into cathepsin functions have been made possible by the generation of knockout mice and by the application of specific inhibitors. Inflammatory cytokines regulate the expression and activities of cathepsins in cultured vascular cells and macrophages. In addition, evaluations of the possibility of cathepsins as a diagnostic tool revealed that the circulating levels of cathepsin S, K, and L, and their endogenous inhibitor cystatin C could be promising biomarkers in the diagnosis of coronary artery disease, aneurysm, adiposity, peripheral arterial disease, and coronary artery calcification. In this review, we summarize the available information regarding the mechanistic contributions of cathepsins to ASCVD.

Indexed as

AnimalsAtherosclerosisCardiovascular DiseasesCathepsinsHumansCathepsinsAneurysmAtherosclerosisCathepsinsNeovascularizationRestenosis

Identifiers

PMID28978867
PMCPMC5827079

What OpenQuestion holds

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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.