Evidence map›Paper›PMID 26543826›Full record

ArticleCardiovascular diagnosis and therapy2015

Boosting autophagy in the diabetic heart: a translational perspective.

Sebastiano Sciarretta, V Subbarao Boppana, Mahaa Umapathi, Giacomo Frati, Junichi Sadoshima

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cardiovascular diagnosis and therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed.

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  16. Role of Autophagy in Lung Inflammation.Frontiers in immunology · 2020
    Review
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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

5 authors.

Sebastiano Sciarretta1 Cardiovascular Research Institute, Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey 07103, USA ; 2 IRCCS Neuromed, Pozzilli (IS) 86077, Italy ; 3 Department of Medical-Surgical Sciences and Biotechnologies, University of Rome "Sapienza", Latina 04100, Italy.
V Subbarao Boppana1 Cardiovascular Research Institute, Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey 07103, USA ; 2 IRCCS Neuromed, Pozzilli (IS) 86077, Italy ; 3 Department of Medical-Surgical Sciences and Biotechnologies, University of Rome "Sapienza", Latina 04100, Italy.
Mahaa Umapathi1 Cardiovascular Research Institute, Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey 07103, USA ; 2 IRCCS Neuromed, Pozzilli (IS) 86077, Italy ; 3 Department of Medical-Surgical Sciences and Biotechnologies, University of Rome "Sapienza", Latina 04100, Italy.
Giacomo Frati1 Cardiovascular Research Institute, Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey 07103, USA ; 2 IRCCS Neuromed, Pozzilli (IS) 86077, Italy ; 3 Department of Medical-Surgical Sciences and Biotechnologies, University of Rome "Sapienza", Latina 04100, Italy.
Junichi Sadoshima1 Cardiovascular Research Institute, Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey 07103, USA ; 2 IRCCS Neuromed, Pozzilli (IS) 86077, Italy ; 3 Department of Medical-Surgical Sciences and Biotechnologies, University of Rome "Sapienza", Latina 04100, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes, obesity, and dyslipidemia are main risk factors that promote the development of cardiovascular diseases. These metabolic abnormalities are frequently found to be associated together in a highly morbid clinical condition called metabolic syndrome. Metabolic derangements promote endothelial dysfunction, atherosclerotic plaque formation and rupture, cardiac remodeling and dysfunction. This evidence strongly encourages the elucidation of the mechanisms through which obesity, diabetes, and metabolic syndrome induce cellular abnormalities and dysfunction in order to discover new therapeutic targets and strategies for their prevention and treatment. Numerous studies employing both dietary and genetic animal models of obesity and diabetes have demonstrated that autophagy, an intracellular system for protein degradation, is impaired in the heart under these conditions. This suggests that autophagy reactivation may represent a future potential therapeutic intervention to reduce cardiac maladaptive alterations in patients with metabolic derangements. In fact, autophagy is a critical mechanism to preserve cellular homeostasis and survival. In addition, the physiological activation of autophagy protects the heart during stress, such as acute ischemia, starvation, chronic myocardial infarction, pressure overload, and proteotoxic stress. All these aspects will be discussed in our review article together with the potential ways to reactivate autophagy in the context of obesity, metabolic syndrome, and diabetes.

Indexed as

Autophagydiabetesheartmetabolic syndromeobesity

Identifiers

PMID26543826
PMCPMC4609904

What OpenQuestion holds

Textmetadata
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.