Evidence map›Paper›PMID 30766511›Full record

ReviewFrontiers in endocrinology2018

Chaperone Mediated Autophagy in the Crosstalk of Neurodegenerative Diseases and Metabolic Disorders.

Iván E Alfaro, Amelina Albornoz, Alfredo Molina, José Moreno, Karina Cordero, Alfredo Criollo, Mauricio Budini

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
9.7field-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

60 citing papers in PubMed, 93 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

7 authors at 3 institutions in 1 country.

Iván E AlfaroFundación Ciencia & Vida, Santiago, Chile.
Amelina AlbornozFundación Ciencia & Vida, Santiago, Chile.
Alfredo MolinaDentistry Faculty, Institute in Dentistry Sciences, University of Chile, Santiago, Chile.
José MorenoDentistry Faculty, Institute in Dentistry Sciences, University of Chile, Santiago, Chile.
Karina CorderoDentistry Faculty, Institute in Dentistry Sciences, University of Chile, Santiago, Chile.
Alfredo CriolloDentistry Faculty, Institute in Dentistry Sciences, University of Chile, Santiago, Chile.
Mauricio BudiniDentistry Faculty, Institute in Dentistry Sciences, University of Chile, Santiago, Chile.
University of Chile · CLFundación Ciencia and Vida · CLAdvanced Center for Chronic Diseases · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chaperone Mediated Autophagy (CMA) is a lysosomal-dependent protein degradation pathway. At least 30% of cytosolic proteins can be degraded by this process. The two major protein players of CMA are LAMP-2A and HSC70. While LAMP-2A works as a receptor for protein substrates at the lysosomal membrane, HSC70 specifically binds protein targets and takes them for CMA degradation. Because of the broad spectrum of proteins able to be degraded by CMA, this pathway has been involved in physiological and pathological processes such as lipid and carbohydrate metabolism, and neurodegenerative diseases, respectively. Both, CMA, and the mentioned processes, are affected by aging and by inadequate nutritional habits such as a high fat diet or a high carbohydrate diet. Little is known regarding about CMA, which is considered a common regulation factor that links metabolism with neurodegenerative disorders. This review summarizes what is known about CMA, focusing on its molecular mechanism, its role in protein, lipid and carbohydrate metabolism. In addition, the review will discuss how CMA could be linked to protein, lipids and carbohydrate metabolism within neurodegenerative diseases. Furthermore, it will be discussed how aging and inadequate nutritional habits can have an impact on both CMA activity and neurodegenerative disorders.

Indexed as

carbohydratesCMAlipidsmetabolismneurodegeneration

Identifiers

PMID30766511
PMCPMC6365421
OpenAlexW2911661890

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.