Evidence map›Paper›PMID 28246200›Full record

ReviewScience signaling2017

Target acquired: Selective autophagy in cardiometabolic disease.

Trent D Evans, Ismail Sergin, Xiangyu Zhang, Babak Razani

Abstract readReview
In one paragraph

Review in Science signaling, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

38 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Trehalose promotes atherosclerosis regression in female mice.Frontiers in cardiovascular medicine · 2024
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. HApoptosis : an international journal on programmed cell death · 2021
    Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. Review
  20. Article
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

4 authors at 1 institution in 1 country.

Trent D EvansCardiovascular Division, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.ORCID 0000-0003-1809-444X
Ismail SerginCardiovascular Division, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Xiangyu ZhangCardiovascular Division, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Babak RazaniCardiovascular Division, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA. brazani@im.wustl.edu.ORCID 0000-0002-7172-9240
Washington University in St. Louis · US

Funding

Washington University Nutrition Obesity Research CenterP30DK056341 · NIDDK · WASHINGTON UNIVERSITY · PI Dominic N Reeds · 1999 to 2026
$30.2M
WU P&FP30DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI Irfan J Lodhi · 2013 to 2026
$27.1M
THE ROLE OF MACROPHAGE LYSOSOMAL BIOGENESIS IN ATHEROSCLEROSISR01HL125838 · NHLBI · WASHINGTON UNIVERSITY · PI RAZANI, BABAK · 2015 to 2025
$4.6M
Characterization of a Lysosomal Acid Lipase Variant Associated with Coronary DiseaseF31HL132434 · NHLBI · WASHINGTON UNIVERSITY · PI EVANS, TRENT · 2016 to 2019
$114k
NHLBI NIH HHS F31 HL132434NHLBI NIH HHS R01 HL125838NIDDK NIH HHS P30 DK020579NIDDK NIH HHS P30 DK056341
6 · The paper itself

Abstract

The accumulation of damaged or excess proteins and organelles is a defining feature of metabolic disease in nearly every tissue. Thus, a central challenge in maintaining metabolic homeostasis is the identification, sequestration, and degradation of these cellular components, including protein aggregates, mitochondria, peroxisomes, inflammasomes, and lipid droplets. A primary route through which this challenge is met is selective autophagy, the targeting of specific cellular cargo for autophagic compartmentalization and lysosomal degradation. In addition to its roles in degradation, selective autophagy is emerging as an integral component of inflammatory and metabolic signaling cascades. In this Review, we focus on emerging evidence and key questions about the role of selective autophagy in the cell biology and pathophysiology of metabolic diseases such as obesity, diabetes, atherosclerosis, and steatohepatitis. Essential players in these processes are the selective autophagy receptors, defined broadly as adapter proteins that both recognize cargo and target it to the autophagosome. Additional domains within these receptors may allow integration of information about autophagic flux with critical regulators of cellular metabolism and inflammation. Details regarding the precise receptors involved, such as p62 and NBR1, and their predominant interacting partners are just beginning to be defined. Overall, we anticipate that the continued study of selective autophagy will prove to be informative in understanding the pathogenesis of metabolic diseases and to provide previously unrecognized therapeutic targets.

Indexed as

AutophagyAtherosclerosisAutophagosomesDiabetes MellitusFatty LiverHumansModels, BiologicalObesitySequestosome-1 ProteinSignal TransductionSequestosome-1 Protein

Identifiers

PMID28246200
PMCPMC5451512
OpenAlexW2591995673

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.