Evidence map›Paper›PMID 32664529›Full record

ReviewInternational journal of molecular sciences2020

Aortic Valve Stenosis and Mitochondrial Dysfunctions: Clinical and Molecular Perspectives.

Gaia Pedriali, Giampaolo Morciano, Simone Patergnani, Paolo Cimaglia, Cristina Morelli, Elisa Mikus, Roberto Ferrari, Vincenzo Gasbarro, Carlotta Giorgi, Mariusz R Wieckowski and 1 more

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.0field-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

29 citing papers in PubMed, 35 citations in OpenAlex.

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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

11 authors at 4 institutions in 2 countries.

Gaia PedrialiMaria Cecilia Hospital, GVM Care & Research, Cotignola, 48033 Ravenna, Italy.
Giampaolo MorcianoMaria Cecilia Hospital, GVM Care & Research, Cotignola, 48033 Ravenna, Italy.
Simone PatergnaniMaria Cecilia Hospital, GVM Care & Research, Cotignola, 48033 Ravenna, Italy.ORCID 0000-0001-7951-9267
Paolo CimagliaCardiovascular Department, Maria Cecilia Hospital, GVM Care & Research, Cotignola, 48033 Ravenna, Italy.
Cristina MorelliCardiology Unit, Azienda Ospedaliero Universitaria di Ferrara, 44121 Ferrara, Italy.
Elisa MikusCardiovascular Department, Maria Cecilia Hospital, GVM Care & Research, Cotignola, 48033 Ravenna, Italy.
Roberto FerrariMaria Cecilia Hospital, GVM Care & Research, Cotignola, 48033 Ravenna, Italy.
Vincenzo GasbarroDepartment of Medical Sciences, Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, 44121 Ferrara, Italy.
Carlotta GiorgiDepartment of Medical Sciences, Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, 44121 Ferrara, Italy.
Mariusz R WieckowskiLaboratory of Mitochondrial Biology and Metabolism, Nencki Institute of Experimental Biology, Pasteur 3, 02-093 Warsaw, Poland.
Paolo PintonMaria Cecilia Hospital, GVM Care & Research, Cotignola, 48033 Ravenna, Italy.
University of Ferrara · ITMaria Cecilia Hospital · ITArcispedale Sant'Anna · ITInstytut Biologii Doświadczalnej im. Marcelego Nenckiego · PL

Funding

Associazione Italiana per la Ricerca sul Cancro IG-19803Associazione Italiana per la Ricerca sul Cancro IG-23670European Research Council ERC, 853057Fondazione Telethon GGP11139BItalian Ministry of Health GR-2013-02356747Progetti di Rilevante Interesse Nazionale 2017 7E9EPYProgetti di Rilevante Interesse Nazionale 2017 E5L5P3
6 · The paper itself

Abstract

Calcific aortic stenosis is a disorder that impacts the physiology of heart valves. Fibrocalcific events progress in conjunction with thickening of the valve leaflets. Over the years, these events promote stenosis and obstruction of blood flow. Known and common risk factors are congenital defects, aging and metabolic syndromes linked to high plasma levels of lipoproteins. Inflammation and oxidative stress are the main molecular mediators of the evolution of aortic stenosis in patients and these mediators regulate both the degradation and remodeling processes. Mitochondrial dysfunction and dysregulation of autophagy also contribute to the disease. A better understanding of these cellular impairments might help to develop new ways to treat patients since, at the moment, there is no effective medical treatment to diminish neither the advancement of valve stenosis nor the left ventricular function impairments, and the current approaches are surgical treatment or transcatheter aortic valve replacement with prosthesis.

Indexed as

AnimalsAortic ValveAortic Valve StenosisAutophagyBasement MembraneCalcinosisDisease ProgressionEndothelial CellsHumansInflammationLipidsMitochondria, HeartNitric Oxide Synthase Type IIIOxidative StressTherapies, InvestigationalUnfolded Protein ResponseLipidsNitric Oxide Synthase Type IIINOS3 protein, humanAortic stenosisautophagycardiovascular diseaseinflammationmitochondria

Identifiers

PMID32664529
PMCPMC7402290
OpenAlexW3041993950

What OpenQuestion holds

Textmetadata
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.