Evidence mapPaperPMID 37531253Full record

ArticleCell reports2023

Pericyte dysfunction and impaired vasomotion are hallmarks of islets during the pathogenesis of type 1 diabetes.

Luciana Mateus Gonçalves, Mirza Muhammad Fahd Qadir, Maria Boulina, Madina Makhmutova, Elizabeth Pereira, Joana Almaça

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
8.6field-weighted citation impact, top 2% 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

22 citing papers in PubMed, 27 citations in OpenAlex.

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  20. Diabetes as a Pancreatic Microvascular Disease-A Pericytic Perspective.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2024
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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

6 authors at 2 institutions in 1 country.

Luciana Mateus GonçalvesDivision of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Miami Miller School of Medicine, Miami, FL, USA.
Mirza Muhammad Fahd QadirSection of Endocrinology and Metabolism, John W. Deming Department of Medicine, Tulane University School of Medicine, New Orleans, LA, USA; Southeast Louisiana Veterans Health Care System, New Orleans, LA, USA; Tulane Center of Excellence in Sex-Based Biology & Medicine, New Orleans, LA, USA.
Maria BoulinaDiabetes Research Institute, University of Miami, Miami, FL, USA.
Madina MakhmutovaDivision of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Miami Miller School of Medicine, Miami, FL, USA.
Elizabeth PereiraDivision of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Miami Miller School of Medicine, Miami, FL, USA; Department of Physiology and Biophysics, University of Miami Miller School of Medicine, Miami, FL, USA.
Joana AlmaçaDivision of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Miami Miller School of Medicine, Miami, FL, USA; Department of Physiology and Biophysics, University of Miami Miller School of Medicine, Miami, FL, USA; Molecular and Cellular Pharmacology Graduate Program, University of Miami Miller School of Medicine, Miami, FL, USA. Electronic address: jalmaca@med.miami.edu.
University of Miami · USTulane University · US

Funding

The Human Pancreas Analysis Program for Type 2 DiabetesU01DK123594 · NIDDK · UNIVERSITY OF PENNSYLVANIA · 2022 to 2025
$8.0M
Renewal of the Human Islet Research Enhancement Center (HIREC) for the Type-1-Diabetes-Focused Human Islet Research Network (HIRN).U24DK104162 · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · 2025 to 2025
$1.6M
Human Pancreas Analysis Program-T2DU01DK123716 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MARK A. ATKINSON, Rita Bottino · 2022 to 2022
$1.1M
Investigating the link between pericyte dysfunction and loss of glucose homeostasis in COVID-19R01DK133483 · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · 2025 to 2025
$384k
NIDDK NIH HHS K01 DK111757NIDDK NIH HHS R01 DK133483NIDDK NIH HHS U01 DK104162NIDDK NIH HHS U01 DK123594NIDDK NIH HHS U01 DK123716NIDDK NIH HHS U24 DK104162NIDDK NIH HHS UC4 DK112217NIDDK NIH HHS UC4 DK112232
6 · The paper itself

Abstract

Pancreatic islets are endocrine organs that depend on their microvasculature to function. Along with endothelial cells, pericytes comprise the islet microvascular network. These mural cells are crucial for microvascular stability and function, but it is not known if/how they are affected during the development of type 1 diabetes (T1D). Here, we investigate islet pericyte density, phenotype, and function using living pancreas slices from donors without diabetes, donors with a single T1D-associated autoantibody (GADA+), and recent onset T1D cases. Our data show that islet pericyte and capillary responses to vasoactive stimuli are impaired early on in T1D. Microvascular dysfunction is associated with a switch in the phenotype of islet pericytes toward myofibroblasts. Using publicly available RNA sequencing (RNA-seq) data, we further found that transcriptional alterations related to endothelin-1 signaling and vascular and extracellular matrix (ECM) remodeling are hallmarks of single autoantibody (Aab)+ donor pancreata. Our data show that microvascular dysfunction is present at early stages of islet autoimmunity.

Indexed as

Diabetes Mellitus, Type 1Islets of LangerhansAutoantibodiesEndothelial CellsHumansPericytesAutoantibodiescapillary diameterCP: Cell biologyCP: Metabolismendothelin-1microvasculaturemyofibroblastpancreatic isletpericytesRNA-seqsympathetic nervestype 1 diabetesvasomotion

Identifiers

PMID37531253
PMCPMC10529889
OpenAlexW4385454023

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.