Evidence map›Paper›PMID 30483501›Full record

ReviewFrontiers in cell and developmental biology2018

Selective Autophagy and Xenophagy in Infection and Disease.

Vartika Sharma, Surbhi Verma, Elena Seranova, Sovan Sarkar, Dhiraj Kumar

Abstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 154 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
154citing papers in PubMed, 2 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

154 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Review
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  5. Article
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  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. mBio · 2025
    Article
  14. HEATR3 recognizes membrane rupture and facilitates xenophagy in response toProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  15. Article
  16. Review
  17. Review
  18. Editorial: The role of autophagy in infectious diseases, volume II.Frontiers in cellular and infection microbiology · 2025
    Article
  19. Article
  20. Article

94 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

5 authors.

Vartika SharmaCellular Immunology Group, International Centre for Genetic Engineering and Biotechnology, New Delhi, India.
Surbhi VermaCellular Immunology Group, International Centre for Genetic Engineering and Biotechnology, New Delhi, India.
Elena SeranovaInstitute of Cancer and Genomic Sciences, Institute of Biomedical Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom.
Sovan SarkarInstitute of Cancer and Genomic Sciences, Institute of Biomedical Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom.
Dhiraj KumarCellular Immunology Group, International Centre for Genetic Engineering and Biotechnology, New Delhi, India.

Funding

DBT-Wellcome Trust India Alliance IA/S/17/1/503071
6 · The paper itself

Abstract

Autophagy, a cellular homeostatic process, which ensures cellular survival under various stress conditions, has catapulted to the forefront of innate defense mechanisms during intracellular infections. The ability of autophagy to tag and target intracellular pathogens toward lysosomal degradation is central to this key defense function. However, studies involving the role and regulation of autophagy during intracellular infections largely tend to ignore the housekeeping function of autophagy. A growing number of evidences now suggest that the housekeeping function of autophagy, rather than the direct pathogen degradation function, may play a decisive role to determine the outcome of infection and immunological balance. We discuss herein the studies that establish the homeostatic and anti-inflammatory function of autophagy, as well as role of bacterial effectors in modulating and coopting these functions. Given that the core autophagy machinery remains largely the same across diverse cargos, how selectivity plays out during intracellular infection remains intriguing. We explore here, the contrasting role of autophagy adaptors being both selective as well as pleotropic in functions and discuss whether E3 ligases could bring in the specificity to cargo selectivity.

Indexed as

DUBsinflammationNDP52OPTNp62TAX1BP1ubiquitinationxenophagy

Identifiers

PMID30483501
PMCPMC6243101

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.