Evidence map›Paper›PMID 34508250›Full record

ReviewNature reviews. Endocrinology2021

Autophagy in metabolic disease and ageing.

Munehiro Kitada, Daisuke Koya

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 228 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
228citing papers in PubMed, 2 pooled it
40.2field-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

228 citing papers in PubMed, 2 syntheses or guidelines pooled it, 376 citations in OpenAlex.

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168 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Munehiro KitadaDepartment of Diabetology and Endocrinology, Kanazawa Medical University, Uchinada, Ishikawa, Japan.ORCID http://orcid.org/0000-0002-3854-1385
Daisuke KoyaDepartment of Diabetology and Endocrinology, Kanazawa Medical University, Uchinada, Ishikawa, Japan. koya0516@kanazawa-med.ac.jp.ORCID http://orcid.org/0000-0003-2711-1539
Kanazawa Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is an evolutionarily conserved, lysosome-dependent catabolic process whereby cytoplasmic components, including damaged organelles, protein aggregates and lipid droplets, are degraded and their components recycled. Autophagy has an essential role in maintaining cellular homeostasis in response to intracellular stress; however, the efficiency of autophagy declines with age and overnutrition can interfere with the autophagic process. Therefore, conditions such as sarcopenic obesity, insulin resistance and type 2 diabetes mellitus (T2DM) that are characterized by metabolic derangement and intracellular stresses (including oxidative stress, inflammation and endoplasmic reticulum stress) also involve the accumulation of damaged cellular components. These conditions are prevalent in ageing populations. For example, sarcopenia is an age-related loss of skeletal muscle mass and strength that is involved in the pathogenesis of both insulin resistance and T2DM, particularly in elderly people. Impairment of autophagy results in further aggravation of diabetes-related metabolic derangements in insulin target tissues, including the liver, skeletal muscle and adipose tissue, as well as in pancreatic β-cells. This Review summarizes the role of autophagy in the pathogenesis of metabolic diseases associated with or occurring in the context of ageing, including insulin resistance, T2DM and sarcopenic obesity, and describes its potential as a therapeutic target.

Indexed as

AutophagyAgedAgingDiabetes Mellitus, Type 2HumansInsulin ResistanceMetabolic DiseasesObesitySarcopenia

Identifiers

PMID34508250
OpenAlexW3197868296

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.