Evidence map›Paper›PMID 27334205›Full record

ReviewNature reviews. Rheumatology2016

Autophagy: controlling cell fate in rheumatic diseases.

Jason S Rockel, Mohit Kapoor

Erratum issuedAbstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Rheumatology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
12.9field-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

69 citing papers in PubMed, 156 citations in OpenAlex.

  1. Article
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  8. Defining Mechanistic Links Between the Non-Coding Variant rs17673553 inInternational journal of molecular sciences · 2025
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9 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Jason S RockelArthritis Program, Toronto Western Hospital, University Health Network, 399 Bathurst Street, Toronto, Ontario, M5T 2S8, Canada.
Mohit KapoorArthritis Program, Toronto Western Hospital, University Health Network, 399 Bathurst Street, Toronto, Ontario, M5T 2S8, Canada.
Toronto Western Hospital · CA

Funding

CIHR 126016
6 · The paper itself

Abstract

Autophagy, an endogenous process necessary for the turnover of organelles, maintains cellular homeostasis and directs cell fate. Alterations to the regulation of autophagy contribute to the progression of various rheumatic diseases, including systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), osteoarthritis (OA) and systemic sclerosis (SSc). Implicit in the progression of these diseases are cell-type-specific responses to surrounding factors that alter autophagy: chondrocytes within articular cartilage show decreased autophagy in OA, leading to rapid cell death and cartilage degeneration; fibroblasts from patients with SSc have restricted autophagy, similar to that seen in aged dermal fibroblasts; fibroblast-like synoviocytes from RA joints show altered autophagy, which contributes to synovial hyperplasia; and dysregulation of autophagy in haematopoietic lineage cells alters their function and maturation in SLE. Various upstream mechanisms also contribute to these diseases by regulating autophagy as part of their signalling cascades. In this Review, we discuss the links between autophagy, immune responses, fibrosis and cellular fates as they relate to pathologies associated with rheumatic diseases. Therapies in clinical use, and in preclinical or clinical development, are also discussed in relation to their effects on autophagy in rheumatic diseases.

Indexed as

AutophagyAnimalsAntibodies, MonoclonalAutophagy-Related ProteinsDrug Therapy, CombinationLupus Erythematosus, SystemicRheumatic DiseasesScleroderma, SystemicTOR Serine-Threonine KinasesAntibodies, MonoclonalAutophagy-Related ProteinsTOR Serine-Threonine Kinases

Identifiers

PMID27334205
OpenAlexW2466888597

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.