Evidence map›Paper›PMID 33881501›Full record

ReviewCardiovascular research2022

Role of oxidative stress in calcific aortic valve disease and its therapeutic implications.

Harry Z E Greenberg, Guoan Zhao, Ajay M Shah, Min Zhang

Registry-linked trialOpen access · hybridAbstract readReview
In one paragraph

Review in Cardiovascular research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05875675 (Effect of Pioglitazone Treatment in Patient's Calcific Aortic Valve Disease With Mild Aortic Valve Stenosis), which is not on this map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
9.9field-weighted citation impact, top 1% 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.

NCT05875675 phase2not yet recruitingnot on this mapstarted 2023, after this paper: background citation

Effect of Pioglitazone Treatment in Patient's Calcific Aortic Valve Disease With Mild Aortic Valve Stenosis

TypeinterventionalSponsorUnion Hospital, Tongji Medical College, Huazhong University of Science and TechnologyRan2023 to 2028Enrolled100ConditionsCalcification of Aortic Valve, Aortic Valve StenosisArmsDrug: Pioglitazone Oral Tablet, Placebo
3 · Its place in the literature

Who cites it

64 citing papers in PubMed, 103 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Observational
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

4 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 2 countries.

Harry Z E GreenbergDepartment of Cardiology, Cardiovascular Division, King's College London British Heart Foundation Centre of Research Excellence, James Black Centre, 125 Coldharbour Lane, London SE5 9NU, UK.
Guoan ZhaoDepartment of Cardiology, The First Affiliated Hospital of Xinxiang Medical University, Heart Center of Xinxiang Medical University, Henan, China.
Ajay M ShahDepartment of Cardiology, Cardiovascular Division, King's College London British Heart Foundation Centre of Research Excellence, James Black Centre, 125 Coldharbour Lane, London SE5 9NU, UK.ORCID 0000-0002-6547-0631
Min ZhangDepartment of Cardiology, Cardiovascular Division, King's College London British Heart Foundation Centre of Research Excellence, James Black Centre, 125 Coldharbour Lane, London SE5 9NU, UK.ORCID 0000-0003-1657-1337
King's College London · GBFirst Affiliated Hospital of Xinxiang Medical University · CN

Funding

British Heart Foundation CH/1999001/11735British Heart Foundation PG/17/39/33027
6 · The paper itself

Abstract

Calcific aortic valve disease (CAVD) is the end result of active cellular processes that lead to the progressive fibrosis and calcification of aortic valve leaflets. In western populations, CAVD is a significant cause of cardiovascular morbidity and mortality, and in the absence of effective drugs, it will likely represent an increasing disease burden as populations age. As there are currently no pharmacological therapies available for preventing, treating, or slowing the development of CAVD, understanding the mechanisms underlying the initiation and progression of the disease is important for identifying novel therapeutic targets. Recent evidence has emerged of an important causative role for reactive oxygen species (ROS)-mediated oxidative stress in the pathophysiology of CAVD, inducing the differentiation of valve interstitial cells into myofibroblasts and then osteoblasts. In this review, we focus on the roles and sources of ROS driving CAVD and consider their potential as novel therapeutic targets for this debilitating condition.

Indexed as

Aortic ValveAortic Valve StenosisCalcinosisHumansOxidative StressReactive Oxygen SpeciesReactive Oxygen SpeciesAortic valveCalcificationNADPH oxidasesOxidative stressReactive oxygen species

Identifiers

PMID33881501
PMCPMC9074995
OpenAlexW3155763441

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.