Evidence map›Paper›PMID 33255983›Full record

ReviewInternational journal of molecular sciences2020

Autophagy and Autophagy-Related Diseases: A Review.

Tadashi Ichimiya, Tsukasa Yamakawa, Takehiro Hirano, Yoshihiro Yokoyama, Yuki Hayashi, Daisuke Hirayama, Kohei Wagatsuma, Takao Itoi, Hiroshi Nakase

Abstract readReview
In one paragraph

Review 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 180 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
180citing papers in PubMed, 5 pooled it
–field-weighted citation impact
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

180 citing papers in PubMed, 5 syntheses or guidelines pooled it.

  1. Pooled it
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  6. Review
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  8. From lipid overload to autophagy collapse: how lipid dysregulation drives chronic inflammation and metabolic disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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120 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

9 authors.

Tadashi IchimiyaDepartment of Gastroenterology and Hepatology, Sapporo Medical University School of Medicine, Sapporo 060-8543, Japan.
Tsukasa YamakawaDepartment of Gastroenterology and Hepatology, Sapporo Medical University School of Medicine, Sapporo 060-8543, Japan.
Takehiro HiranoDepartment of Gastroenterology and Hepatology, Sapporo Medical University School of Medicine, Sapporo 060-8543, Japan.
Yoshihiro YokoyamaDepartment of Gastroenterology and Hepatology, Sapporo Medical University School of Medicine, Sapporo 060-8543, Japan.ORCID 0000-0003-2434-1048
Yuki HayashiDepartment of Gastroenterology and Hepatology, Sapporo Medical University School of Medicine, Sapporo 060-8543, Japan.
Daisuke HirayamaDepartment of Gastroenterology and Hepatology, Sapporo Medical University School of Medicine, Sapporo 060-8543, Japan.ORCID 0000-0002-9842-4850
Kohei WagatsumaDepartment of Gastroenterology and Hepatology, Sapporo Medical University School of Medicine, Sapporo 060-8543, Japan.ORCID 0000-0002-6774-7868
Takao ItoiDepartment of Gastroenterology and Hepatology, Tokyo Medical University, Tokyo 160-0023, Japan.
Hiroshi NakaseDepartment of Gastroenterology and Hepatology, Sapporo Medical University School of Medicine, Sapporo 060-8543, Japan.ORCID 0000-0003-2848-6586

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy refers to the process involving the decomposition of intracellular components via lysosomes. Autophagy plays an important role in maintaining and regulating cell homeostasis by degrading intracellular components and providing degradation products to cells. In vivo, autophagy has been shown to be involved in the starvation response, intracellular quality control, early development, and cell differentiation. Recent studies have revealed that autophagy dysfunction is implicated in neurodegenerative diseases and tumorigenesis. In addition to the discovery of certain disease-causing autophagy-related mutations and elucidation of the pathogenesis of conditions resulting from the abnormal degradation of selective autophagy substrates, the activation of autophagy is essential for prolonging life and suppressing aging. This article provides a comprehensive review of the role of autophagy in health, physiological function, and autophagy-related disease.

Indexed as

AutophagyDiseaseAnimalsHealthHumansMechanistic Target of Rapamycin Complex 1Models, BiologicalMechanistic Target of Rapamycin Complex 1autophagyautophagy-related genecancercardiovascularliver diseasemitophagyneurodegenerative disease

Identifiers

PMID33255983
PMCPMC7729615

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.