Evidence map›Paper›PMID 32623955›Full record

ReviewThe journal of histochemistry and cytochemistry : official journal of the Histochemistry Society2020

Proteoglycan-driven Autophagy: A Nutrient-independent Mechanism to Control Intracellular Catabolism.

Thomas Neill, Simone Buraschi, Aastha Kapoor, Renato V Iozzo

Open access · bronzeAbstract readReview
In one paragraph

Review in The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. A functional outside-in signaling network of proteoglycans and matrix molecules regulating autophagy.Matrix biology : journal of the International Society for Matrix Biology · 2021
    Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. 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.

Thomas NeillDepartment of Pathology, Anatomy & Cell Biology, Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA.
Simone BuraschiDepartment of Pathology, Anatomy & Cell Biology, Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA.
Aastha KapoorDepartment of Pathology, Anatomy & Cell Biology, Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA.
Renato V IozzoDepartment of Pathology, Anatomy & Cell Biology, Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA.
Thomas Jefferson University · US

Funding

NEOPLASTIC MODULATION OF PROTEOGLYCAN METABOLISMR01CA039481 · NCI · UNIVERSITY OF PENNSYLVANIA · PI IOZZO, RENATO V. · 1985 to 2020
$7.1M
The Biology of Perlecan in Cancer and AngiogenesisR01CA047282 · NCI · THOMAS JEFFERSON UNIVERSITY · PI IOZZO, RENATO V. · 1990 to 2019
$5.7M
NCI NIH HHS R01 CA039481NCI NIH HHS R01 CA047282
6 · The paper itself

Abstract

Proteoglycans are rapidly emerging as versatile regulators of intracellular catabolic pathways. This is predominantly achieved via the non-canonical induction of autophagy, a fundamentally and evolutionarily conserved eukaryotic pathway necessary for maintaining organismal homeostasis. Autophagy facilitated by either decorin, a small leucine-rich proteoglycan, or perlecan, a basement membrane heparan sulfate proteoglycan, proceeds independently of ambient nutrient conditions. We found that soluble decorin evokes endothelial cell autophagy and breast carcinoma cell mitophagy by directly interacting with vascular endothelial growth factor receptor 2 (VEGFR2) or the Met receptor tyrosine kinase, respectively. Endorepellin, a soluble, proteolytic fragment of perlecan, induces autophagy and endoplasmic reticulum stress within the vasculature, downstream of VEGFR2. These potent matrix-derived cues transduce key biological information via receptor binding to converge upon a newly discovered nexus of core autophagic machinery comprised of Peg3 (paternally expressed gene 3) for autophagy or mitostatin for mitophagy. Here, we give a mechanistic overview of the nutrient-independent, proteoglycan-driven programs utilized for autophagic or mitophagic progression. We propose that catabolic control of cell behavior is an underlying basis for proteoglycan versatility and may provide novel therapeutic targets for the treatment of human disease.

Indexed as

AutophagyAnimalsHumansIntracellular SpaceNutrientsProteoglycansVascular Endothelial Growth Factor Receptor-2NutrientsProteoglycansVascular Endothelial Growth Factor Receptor-2autophagydecorinendorepellinextracellular matrixglycosaminoglycan proteoglycanmitophagymitostatinPeg3perlecan

Identifiers

PMID32623955
PMCPMC7649965
OpenAlexW3039869496

What Socratic 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 Socratic graph.