Evidence map›Paper›PMID 32015340›Full record

ReviewCell death & disease2020

Autophagy in metabolic syndrome: breaking the wheel by targeting the renin-angiotensin system.

Kalhara R Menikdiwela, Latha Ramalingam, Fahmida Rasha, Shu Wang, Jannette M Dufour, Nishan S Kalupahana, Karen K S Sunahara, Joilson O Martins, Naima Moustaid-Moussa

Open access · goldAbstract readReview
In one paragraph

Review in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
8.4field-weighted citation impact, top 2% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.

  1. Pooled it
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  4. The Use of Organoid Cultures in Advancing Nutrition Research.Advances in nutrition (Bethesda, Md.) · 2025
    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

9 authors at 3 institutions in 3 countries.

Kalhara R MenikdiwelaDepartment of Nutritional Sciences, Texas Tech University, Lubbock, TX, USA.
Latha RamalingamDepartment of Nutritional Sciences, Texas Tech University, Lubbock, TX, USA.
Fahmida RashaDepartment of Nutritional Sciences, Texas Tech University, Lubbock, TX, USA.
Shu WangDepartment of Nutritional Sciences, Texas Tech University, Lubbock, TX, USA.ORCID http://orcid.org/0000-0001-8078-9942
Jannette M DufourObesity Research Institute, Texas Tech University, Lubbock, TX, USA.
Nishan S KalupahanaDepartment of Nutritional Sciences, Texas Tech University, Lubbock, TX, USA.
Karen K S SunaharaDepartment of Experimental Physiopatholgy, Medical School University of São Paulo, São Paulo, Brazil.
Joilson O MartinsLaboratory of Immunoendocrinology, Department of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences of University Sao Paulo (FCF/USP), São Paulo, Brazil.ORCID http://orcid.org/0000-0003-2630-7038
Naima Moustaid-MoussaDepartment of Nutritional Sciences, Texas Tech University, Lubbock, TX, USA. naima.moustaid-moussa@ttu.edu.ORCID http://orcid.org/0000-0002-7508-8030
Texas Tech University · USUniversidade de São Paulo · BRUniversity of Peradeniya · LK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic syndrome (MetS) is a complex, emerging epidemic which disrupts the metabolic homeostasis of several organs, including liver, heart, pancreas, and adipose tissue. While studies have been conducted in these research areas, the pathogenesis and mechanisms of MetS remain debatable. Lines of evidence show that physiological systems, such as the renin-angiotensin system (RAS) and autophagy play vital regulatory roles in MetS. RAS is a pivotal system known for controlling blood pressure and fluid balance, whereas autophagy is involved in the degradation and recycling of cellular components, including proteins. Although RAS is activated in MetS, the interrelationship between RAS and autophagy varies in glucose homeostatic organs and their cross talk is poorly understood. Interestingly, autophagy is attenuated in the liver during MetS, whereas autophagic activity is induced in adipose tissue during MetS, indicating tissue-specific discordant roles. We discuss in vivo and in vitro studies conducted in metabolic tissues and dissect their tissue-specific effects. Moreover, our review will focus on the molecular mechanisms by which autophagy orchestrates MetS and the ways future treatments could target RAS in order to achieve metabolic homeostasis.

Indexed as

Adipose TissueAutophagyEnergy MetabolismHeart DiseasesHumansInflammationInsulin ResistanceLiverMetabolic SyndromeObesityRenin-Angiotensin System

Identifiers

PMID32015340
PMCPMC6997396
OpenAlexW3003918911

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.