Evidence map›Paper›PMID 32214047›Full record

ReviewJournal of clinical medicine2020

Mitophagy in Cardiovascular Diseases.

Giampaolo Morciano, Simone Patergnani, Massimo Bonora, Gaia Pedriali, Anna Tarocco, Esmaa Bouhamida, Saverio Marchi, Gina Ancora, Gabriele Anania, Mariusz R Wieckowski and 2 more

Open access · goldAbstract readReview
In one paragraph

Review in Journal of clinical medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
10.5field-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.

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

68 citing papers in PubMed, 103 citations in OpenAlex.

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8 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

12 authors at 4 institutions in 2 countries.

Giampaolo MorcianoMaria Cecilia Hospital, GVM Care & Research, Via Corriera 1, Cotignola, 48033 Ravenna, Italy.
Simone PatergnaniMaria Cecilia Hospital, GVM Care & Research, Via Corriera 1, Cotignola, 48033 Ravenna, Italy.
Massimo BonoraDepartment of Medical Sciences, Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, 44121 Ferrara, Italy.
Gaia PedrialiMaria Cecilia Hospital, GVM Care & Research, Via Corriera 1, Cotignola, 48033 Ravenna, Italy.
Anna TaroccoDepartment of Medical Sciences, Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, 44121 Ferrara, Italy.
Esmaa BouhamidaDepartment of Medical Sciences, Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, 44121 Ferrara, Italy.
Saverio MarchiDepartment of Clinical and Molecular Sciences, Marche Polytechnic University, 60126 Ancona, Italy.
Gina AncoraNeonatal Intensive Care Unit, Infermi Hospital Rimini, 47923 Rimini, Italy.
Gabriele AnaniaDepartment of Medical Sciences, Section of General and Thoracic Surgery, University of Ferrara, 44121 Ferrara, Italy.
Mariusz R WieckowskiLaboratory of Mitochondrial Biology and Metabolism, Nencki Institute of Experimental Biology of the Polish Academy of Sciences, 3 Pasteur Str., 02-093 Warsaw, Poland.
Carlotta GiorgiDepartment of Medical Sciences, Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, 44121 Ferrara, Italy.
Paolo PintonMaria Cecilia Hospital, GVM Care & Research, Via Corriera 1, Cotignola, 48033 Ravenna, Italy.
University of Ferrara · ITInstytut Biologii Doświadczalnej im. Marcelego Nenckiego · PLMarche Polytechnic University · ITOspedale Infermi di Rimini · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular diseases are one of the leading causes of death. Increasing evidence has shown that pharmacological or genetic targeting of mitochondria can ameliorate each stage of these pathologies, which are strongly associated with mitochondrial dysfunction. Removal of inefficient and dysfunctional mitochondria through the process of mitophagy has been reported to be essential for meeting the energetic requirements and maintaining the biochemical homeostasis of cells. This process is useful for counteracting the negative phenotypic changes that occur during cardiovascular diseases, and understanding the molecular players involved might be crucial for the development of potential therapies. Here, we summarize the current knowledge on mitophagy (and autophagy) mechanisms in the context of heart disease with an important focus on atherosclerosis, ischemic heart disease, cardiomyopathies, heart failure, hypertension, arrhythmia, congenital heart disease and peripheral vascular disease. We aim to provide a complete background on the mechanisms of action of this mitochondrial quality control process in cardiology and in cardiac surgery by also reviewing studies on the use of known compounds able to modulate mitophagy for cardioprotective purposes.

Indexed as

autophagycardiovascular diseasesmitochondriamitophagy

Identifiers

PMID32214047
PMCPMC7141512
OpenAlexW3013504590

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.