Evidence map›Paper›PMID 22079479›Full record

ReviewExperimental and molecular pathology2012

Autophagy in the brains of young patients with poorly controlled T1DM and fatal diabetic ketoacidosis.

William H Hoffman, John J Shacka, Anuska V Andjelkovic

Open access · greenAbstract readCase ReportsReview
In one paragraph

Review in Experimental and molecular pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

15 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Nutraceutical and Dietary Strategies for Up-Regulating Macroautophagy.International journal of molecular sciences · 2022
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Hyperketonemia (acetoacetate) upregulates NADPH oxidase 4 and elevates oxidative stress, ICAM-1, and monocyte adhesivity in endothelial cells.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2015
    Article
  13. The functional and pathologic relevance of autophagy proteases.The Journal of clinical investigation · 2015
    Review
  14. Diabetes and the brain: oxidative stress, inflammation, and autophagy.Oxidative medicine and cellular longevity · 2014 · on this map
    Review
  15. Review
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

3 authors at 3 institutions in 1 country.

William H HoffmanDepartment of Pediatrics, Section of Pediatric Endocrinology, Georgia Health Sciences University, Augusta, GA, USA. whoffman@georgiahealth.edu
John J Shacka
Anuska V Andjelkovic
Augusta University Health · USUniversity of Alabama at Birmingham · USUniversity of Michigan–Ann Arbor · US

Funding

UAB Neuroscience Core CenterP30NS047466 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI HABLITZ, JOHN J. · 2005 to 2019
$8.5M
The blood brain barrier in neuroinflammationR01NS062853 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ANDJELKOVIC-ZOCHOWSKA, ANUSKA V. · 2009 to 2010
$660k
Cellular Mechanisms of Neuropathology in Parkinson's DiseaseI01BX000957 · VA · BIRMINGHAM VA MEDICAL CENTER · PI SHACKA, JOHN J · 2011 to 2013
–
BLRD VA I01 BX000957NINDS NIH HHS P30 NS047466NINDS NIH HHS P30 NS47466NINDS NIH HHS R01 NS 062853NINDS NIH HHS R01 NS062853
6 · The paper itself

Abstract

Semi-quantitative neuroradiologic studies, quantitative neuron density studies and immunocytochemistry markers of oxidative stress and neuroinflammation indicate neuronal injury and deficits in young patients with chronic poorly controlled type 1 diabetes mellitus (T1DM). Present data suggest that pathogenesis of the neuronal deficits in young patients, who die as the result of diabetic ketoacidosis (DKA) and brain edema (BE), does not involve apoptosis, a prominent form of regulated cell death in many disease states. To further address this we studied mediators of macroautophagy, endoplasmic reticulum (ER) stress and apoptosis. In all areas studied we demonstrated increased levels of macroautophagy-associated proteins including light chain-3 (LC3) and autophagy related protein-4 (Atg4), as well as increased levels of the ER-associated glucose-regulated protein78/binding immunoglobulin protein (GRP78/BiP) in T1DM. In contrast, cleaved caspase-3 was rarely detected in any T1DM brain regions. These results suggest that chronic metabolic instability and oxidative stress may cause alterations in the autophagy-lysosomal pathway but not apoptosis, and macroautophagy-associated molecules may serve as useful candidates for further study in the pathogenesis of early neuronal deficits in T1DM.

Indexed as

AutophagyAdolescentApoptosisAutophagy-Related ProteinsBrain EdemaCysteine EndopeptidasesDiabetes Mellitus, Type 1Diabetic KetoacidosisEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressFatal OutcomeFemaleHeat-Shock ProteinsHumansMicrotubule-Associated ProteinsNeuronsATG4A protein, humanAutophagy-Related ProteinsCysteine EndopeptidasesEndoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsHSPA5 protein, humanMAP1LC3A protein, humanMicrotubule-Associated Proteins

Identifiers

PMID22079479
PMCPMC5557498
OpenAlexW2076312702

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.