Evidence map›Paper›PMID 30653956›Full record

ArticleThe American journal of pathology2019

β1 Syntrophin Supports Autophagy Initiation and Protects against Cerulein-Induced Acute Pancreatitis.

Risheng Ye, Toshiharu Onodera, Pierre-Gilles Blanchard, Christine M Kusminski, Victoria Esser, Rolf A Brekken, Philipp E Scherer

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

4 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. The role of autophagy in pancreatic diseases.Frontiers in pharmacology · 2024
    Review
  3. Article
  4. 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

7 authors at 3 institutions in 1 country.

Risheng YeTouchstone Diabetes Center, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas; Department of Medical Education, Texas Tech University Health Sciences Center Paul L. Foster School of Medicine, El Paso, Texas.
Toshiharu OnoderaTouchstone Diabetes Center, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.
Pierre-Gilles BlanchardTouchstone Diabetes Center, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.
Christine M KusminskiTouchstone Diabetes Center, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.
Victoria EsserDepartment of Biophysics, University of Texas Southwestern Medical Center, Dallas, Texas.
Rolf A BrekkenHamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas, Texas; Department of Surgery, University of Texas Southwestern Medical Center, Dallas, Texas.
Philipp E SchererTouchstone Diabetes Center, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas. Electronic address: philipp.scherer@utsouthwestern.edu.
The University of Texas Southwestern Medical Center · USSouthwestern Medical Center · USTexas Tech University · US

Funding

Novel Mechanisms Regulating the Adipocyte-Brain-Hepatocyte AxisP01DK088761 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI SCHERER, PHILIPP E · 2010 to 2019
$17.4M
Adiponectin, A Protein Secreted From Adipose TissueR01DK055758 · NIDDK · YESHIVA UNIVERSITY · PI SCHERER, PHILIPP E · 2000 to 2024
$10.9M
White Adipose Tissue Physiology, Mitochondrial Function and AdiponectinR01DK099110 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI PHILIPP E SCHERER · 2013 to 2026
$6.7M
NIDDK NIH HHS P01 DK088761NIDDK NIH HHS R01 DK055758NIDDK NIH HHS R01 DK099110
6 · The paper itself

Abstract

Syntrophins are a family of proteins forming membrane-anchored scaffolds and serving as adaptors for various transmembrane and intracellular signaling molecules. To understand the physiological roles of β1 syntrophin, one of the least characterized members, we generated mouse models to eliminate β1 syntrophin specifically in the endocrine or exocrine pancreas. β1 syntrophin is dispensable for the morphology and function of insulin-producing β cells. However, mice with β1 syntrophin deletion in exocrine acinar cells exhibit increased severity of cerulein-induced acute pancreatitis. Reduced expression of cystic fibrosis transmembrane conductance regulator and dilation of acinar lumen are potential predisposition factors. During the disease progression, a relative lack of autophagy is associated with deficiencies in both actin assembly and endoplasmic reticulum nucleation. Our findings reveal, for the first time, that β1 syntrophin is a critical regulator of actin cytoskeleton and autophagy in pancreatic acinar cells and is potently protective against cerulein-induced acute pancreatitis.

Indexed as

AutophagyProtective AgentsAcinar CellsAnimalsCeruletideCystic Fibrosis Transmembrane Conductance RegulatorDystrophin-Associated ProteinsMiceMice, Inbred C57BLMice, KnockoutPancreasPancreatitisCeruletideCftr protein, mouseCystic Fibrosis Transmembrane Conductance RegulatorDystrophin-Associated ProteinsProtective Agentssyntrophin

Identifiers

PMID30653956
PMCPMC6458522
OpenAlexW2910141614

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.