Evidence map›Paper›PMID 27068951›Full record

ReviewBiochemical Society transactions2016

Autophagic degradation of peroxisomes in mammals.

Katarzyna Zientara-Rytter, Suresh Subramani

Open access · greenAbstract readReview
In one paragraph

Review in Biochemical Society transactions, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 2 pooled it
7.6field-weighted citation impact, top 2% 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

39 citing papers in PubMed, 2 syntheses or guidelines pooled it, 63 citations in OpenAlex.

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  18. Selective autophagy as a therapeutic target for neurological diseases.Cellular and molecular life sciences : CMLS · 2021
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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

2 authors at 1 institution in 1 country.

Katarzyna Zientara-RytterSection of Molecular Biology, Division of Biological Sciences, University California, San Diego, CA 92093-0322, U.S.A.
Suresh SubramaniSection of Molecular Biology, Division of Biological Sciences, University California, San Diego, CA 92093-0322, U.S.A. ssubramani@ucsd.edu.
University of California San Diego · US

Funding

TARGETING OF PROTEINS INTO PEROXISOMESR01DK041737 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI AITCHISON, JOHN D., SUBRAMANI, SURESH · 1990 to 2025
$8.4M
Targeting of proteins into peroxisomesR37DK041737 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SUBRAMANI, SURESH · 2004 to 2013
$5.3M
Targeting of Proteins into PeroxisomesR56DK041737 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SUBRAMANI, SURESH · 2014 to 2014
$149k
NIDDK NIH HHS DK41737NIDDK NIH HHS R01 DK041737NIDDK NIH HHS R37 DK041737NIDDK NIH HHS R56 DK041737
6 · The paper itself

Abstract

Peroxisomes are essential organelles required for proper cell function in all eukaryotic organisms. They participate in a wide range of cellular processes including the metabolism of lipids and generation, as well as detoxification, of hydrogen peroxide (H2O2). Therefore, peroxisome homoeostasis, manifested by the precise and efficient control of peroxisome number and functionality, must be tightly regulated in response to environmental changes. Due to the existence of many physiological disorders and diseases associated with peroxisome homoeostasis imbalance, the dynamics of peroxisomes have been widely examined. The increasing volume of reports demonstrating significant involvement of the autophagy machinery in peroxisome removal leads us to summarize current knowledge of peroxisome degradation in mammalian cells. In this review we present current models of peroxisome degradation. We particularly focus on pexophagy-the selective clearance of peroxisomes through autophagy. We also critically discuss concepts of peroxisome recognition for pexophagy, including signalling and selectivity factors. Finally, we present examples of the pathological effects of pexophagy dysfunction and suggest promising future directions.

Indexed as

AutophagyAnimalsHumansMammalsModels, BiologicalPeroxisomesautophagyperoxisomepexophagypexophagy receptor/adaptor

Identifiers

PMID27068951
PMCPMC4958620
OpenAlexW2315094484

What OpenQuestion holds

Textmetadata
LicenceTDM
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.