Evidence map›Paper›PMID 33302427›Full record

ArticleInternational journal of molecular sciences2020

Angiotensin-(1-7) Prevents Lipopolysaccharide-Induced Autophagy via the Mas Receptor in Skeletal Muscle.

Juan Carlos Rivera, Johanna Abrigo, Franco Tacchi, Felipe Simon, Enrique Brandan, Robson A Santos, Michael Bader, Mario Chiong, Claudio Cabello-Verrugio

Open access · goldAbstract read
In one paragraph

Article 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 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 38 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

9 authors at 6 institutions in 3 countries.

Juan Carlos RiveraLaboratory of Muscle Pathology, Fragility and Aging, Department of Biological Sciences, Faculty of Life Sciences, Universidad Andres Bello, Santiago 8370146, Chile.
Johanna AbrigoLaboratory of Muscle Pathology, Fragility and Aging, Department of Biological Sciences, Faculty of Life Sciences, Universidad Andres Bello, Santiago 8370146, Chile.
Franco TacchiLaboratory of Muscle Pathology, Fragility and Aging, Department of Biological Sciences, Faculty of Life Sciences, Universidad Andres Bello, Santiago 8370146, Chile.
Felipe SimonMillennium Institute on Immunology and Immunotherapy, Santiago 8370146, Chile.ORCID 0000-0002-2653-9798
Enrique BrandanCenter for Cell Regulation and Pathology (CRCP), Center for Regeneration and Aging (CARE), Laboratory of Cell Differentiation and Pathology, Department of Cell and Molecular Biology, Faculty of Biological Sciences, P. Universidad Católica de Chile, Santiago 8330077, Chile.
Robson A SantosNational Institute in Science and Technology in Nanobiopharmaceutics, Department of Physiology and Biophysics, Federal University of Minas Gerais (UFMG), Belo Horizonte 31270-901, Brazil.ORCID 0000-0001-8738-5852
Michael BaderMax-Delbrück-Center for Molecular Medicine, 13125 Berlin, Germany.
Mario ChiongAdvanced Center for Chronic DiSeases (ACCDiS), Universidad de Chile, Santiago 8380492, Chile.ORCID 0000-0002-5174-6545
Claudio Cabello-VerrugioLaboratory of Muscle Pathology, Fragility and Aging, Department of Biological Sciences, Faculty of Life Sciences, Universidad Andres Bello, Santiago 8370146, Chile.ORCID 0000-0001-7273-2102
Universidad de Santiago de Chile · CLAdvanced Center for Chronic Diseases · CLMax Delbrück Center · DEPontificia Universidad Católica de Chile · CLUniversidad Andrés Bello · CLUniversidade Federal de Minas Gerais · BR

Funding

Basal grant - CEDENNA from the National Research and Development Agency (ANID), Government of Chile AFB180001Center for Aging and Regeneration (CONICYT, CARE Chile UC AFB170005Conicyt-Ph.D. Scholarship 21141242, 21161353Millennium Institute on Immunology and Immunotherapy P09-016-FMillennium Nucleus of Ion Channels-associated Diseases (MiNICAD) ANIDNational Fund for Science and Technological Development (FONDECYT) 1200944, 1201039, 1190144Programa de Cooperación Científica Ecos-ANID C16S02
6 · The paper itself

Abstract

Skeletal muscle atrophy, which occurs in lipopolysaccharide (LPS)-induced sepsis, causes a severe muscle function reduction. The increased autophagy contributes to sepsis-induced skeletal muscle atrophy in a model of LPS injection, increasing LC3II/LC3I ratio, autophagy flux, and autophagosomes. Angiotensin-(1-7) (Ang-(1-7)) has anti-atrophic effects via the Mas receptor in skeletal muscle. However, the impact of Ang-(1-7) on LPS-induced autophagy is unknown. In this study, we determined the effect of Ang-(1-7) on sepsis-induced muscle autophagy. C57BL6 wild-type (WT) mice and mice lacking the Mas receptor (KO Mas) were injected with LPS together with the systemic administration of Ang-(1-7) to determine autophagy in skeletal muscle. We also evaluated autophagy and p38 and c-Jun N-terminal kinase (JNK)activation. Our results show that Ang-(1-7) prevents LPS-induced autophagy in the diaphragm, tibialis anterior, and gastrocnemius of WT mice, which is demonstrated by a decrease in the LC3II/LC3I ratio and mRNA levels of

Indexed as

AutophagyAngiotensin IAnimalsCathepsin LCell LineLipopolysaccharidesMaleMAP Kinase Kinase 4MiceMice, Inbred C57BLMicrotubule-Associated ProteinsMuscle, Skeletalp38 Mitogen-Activated Protein KinasesPeptide FragmentsProto-Oncogene MasProto-Oncogene ProteinsAngiotensin Iangiotensin I (1-7)Bcl2 protein, mouseCathepsin LCtsl protein, mouseLipopolysaccharidesMap1lc3b protein, mouseMAP Kinase Kinase 4Microtubule-Associated Proteinsp38 Mitogen-Activated Protein KinasesPeptide FragmentsProto-Oncogene MasProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2Receptors, G-Protein-CoupledautophagyLPSmuscle wastingrenin-angiotensin system

Identifiers

PMID33302427
PMCPMC7762589
OpenAlexW3112091833

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.