Evidence map›Paper›PMID 34703273›Full record

ReviewJournal of inflammation research2021

Between Inflammation and Autophagy: The Role of Leptin-Adiponectin Axis in Cardiac Remodeling.

Layla Kamareddine, Crystal M Ghantous, Soumaya Allouch, Sarah A Al-Ashmar, Gulsen Anlar, Surya Kannan, Laiche Djouhri, Hesham M Korashy, Abdelali Agouni, Asad Zeidan

Open access · goldAbstract readReview
In one paragraph

Review in Journal of inflammation research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 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

10 authors at 3 institutions in 4 countries.

Layla KamareddineDepartment Biomedical Sciences, College of Health Sciences, QU Health, Qatar University, Doha, Qatar.
Crystal M GhantousDepartment of Nursing and Health Sciences, Faculty of Nursing and Health Sciences, Notre Dame University-Louaize, Keserwan, Lebanon.
Soumaya AllouchDepartment of Basic Sciences, College of Medicine, QU Health, Qatar University, Doha, Qatar.
Sarah A Al-AshmarBiomedical and Pharmaceutical Research Unit, QU Health, Qatar University, Doha, Qatar.
Gulsen AnlarBiomedical and Pharmaceutical Research Unit, QU Health, Qatar University, Doha, Qatar.
Surya KannanBiomedical and Pharmaceutical Research Unit, QU Health, Qatar University, Doha, Qatar.ORCID 0000-0001-9079-1325
Laiche DjouhriBiomedical and Pharmaceutical Research Unit, QU Health, Qatar University, Doha, Qatar.ORCID 0000-0001-8730-9470
Hesham M KorashyBiomedical and Pharmaceutical Research Unit, QU Health, Qatar University, Doha, Qatar.ORCID 0000-0002-5745-9643
Abdelali AgouniBiomedical and Pharmaceutical Research Unit, QU Health, Qatar University, Doha, Qatar.ORCID 0000-0002-8363-1582
Asad ZeidanBiomedical and Pharmaceutical Research Unit, QU Health, Qatar University, Doha, Qatar.
Qatar University · QANotre Dame University – Louaize · LBQarshi University · PK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac remodeling is the process by which the heart adapts to stressful stimuli, such as hypertension and ischemia/reperfusion; it ultimately leads to heart failure upon long-term exposure. Autophagy, a cellular catabolic process that was originally considered as a mechanism of cell death in response to detrimental stimuli, is thought to be one of the main mechanisms that controls cardiac remodeling and induces heart failure. Dysregulation of the adipokines leptin and adiponectin, which plays essential roles in lipid and glucose metabolism, and in the pathophysiology of the neuroendocrine and cardiovascular systems, has been shown to affect the autophagic response in the heart and to contribute to accelerate cardiac remodeling. The obesity-associated protein leptin is a pro-inflammatory, tumor-promoting adipocytokine whose elevated levels in obesity are associated with acute cardiovascular events, and obesity-related hypertension. Adiponectin exerts anti-inflammatory and anti-tumor effects, and its reduced levels in obesity correlate with the pathogenesis of obesity-associated cardiovascular diseases. Leptin- and adiponectin-induced changes in autophagic flux have been linked to cardiac remodeling and heart failure. In this review, we describe the different molecular mechanisms of hyperleptinemia- and hypoadiponectinemia-mediated pathogenesis of cardiac remodeling and the involvement of autophagy in this process. A better understanding of the roles of leptin, adiponectin, and autophagy in cardiac functions and remodeling, and the exact signal transduction pathways by which they contribute to cardiac diseases may well lead to discovery of new therapeutic agents for the treatment of cardiovascular remodeling.

Indexed as

adiponectinautophagycardiac cellsinflammationleptin

Identifiers

PMID34703273
PMCPMC8528546
OpenAlexW3207152328

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.