Evidence mapPaperPMID 34480875Full record

ReviewThe lancet. Diabetes & endocrinology2021

Restoring normal islet mass and function in type 1 diabetes through regenerative medicine and tissue engineering.

Nicole A J Krentz, Lonnie D Shea, Mark O Huising, James A M Shaw

Open access · greenAbstract readHistorical ArticleReview
In one paragraph

Review in The lancet. Diabetes & endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
5.9field-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

9 citing papers in PubMed, 35 citations in OpenAlex.

  1. Pathogenesis and advances in immunotherapy for type 1 diabetes treatment.Biotechnology reports (Amsterdam, Netherlands) · 2026
    Review
  2. Article
  3. GHRH in diabetes and metabolism.Reviews in endocrine & metabolic disorders · 2025
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. 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

4 authors at 4 institutions in 2 countries.

Nicole A J KrentzDivision of Endocrinology, Department of Pediatrics, Stanford University School of Medicine, Stanford, CA, USA.
Lonnie D SheaDepartments of Biomedical Engineering, Chemical Engineering, and Surgery, College of Engineering and School of Medicine, University of Michigan, Ann Arbor, MI, USA.
Mark O HuisingDepartment of Neurobiology, Physiology and Behavior, College of Biological Sciences, University of California, Davis, Davis, CA, USA; Department of Physiology and Membrane Biology, School of Medicine, University of California, Davis, Davis, CA, USA.
James A M ShawTranslational and Clinical Research Institute, Newcastle University, Newcastle upon Tyne, UK; Institute of Transplantation, Freeman Hospital, Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK. Electronic address: jim.shaw@ncl.ac.uk.
Freeman Hospital · GBStanford University · USUniversity of California, Davis · USUniversity of Michigan–Ann Arbor · US

Funding

Paracrine feedback by pancreatic delta cells to control glucagon and insulin release and manage diabetesR01DK110276 · UNIVERSITY OF CALIFORNIA AT DAVIS · 2025 to 2025
$483k
Minority Predoctiral Fellowship ProgramF31CA110276 · UNIVERSITY OF MARYLAND BALTIMORE · 2005 to 2005
$29k
Medical Research CouncilNCI NIH HHS F31 CA110276NIDDK NIH HHS R01 DK110276NIDDK NIH HHS R01 DK121462Wellcome Trust
6 · The paper itself

Abstract

Type 1 diabetes is characterised by autoimmune-mediated destruction of pancreatic β-cell mass. With the advent of insulin therapy a century ago, type 1 diabetes changed from a progressive, fatal disease to one that requires lifelong complex self-management. Replacing the lost β-cell mass through transplantation has proven successful, but limited donor supply and need for lifelong immunosuppression restricts widespread use. In this Review, we highlight incremental advances over the past 20 years and remaining challenges in regenerative medicine approaches to restoring β-cell mass and function in type 1 diabetes. We begin by summarising the role of endocrine islets in glucose homoeostasis and how this is altered in disease. We then discuss the potential regenerative capacity of the remaining islet cells and the utility of stem cell-derived β-like cells to restore β-cell function. We conclude with tissue engineering approaches that might improve the engraftment, function, and survival of β-cell replacement therapies.

Indexed as

Regenerative MedicineAnimalsCell CountCell ProliferationDiabetes Mellitus, Type 1History, 21st CenturyHumansInsulin-Secreting CellsIslets of LangerhansIslets of Langerhans TransplantationRegenerationTissue Engineering

Identifiers

PMID34480875
PMCPMC10881068
OpenAlexW3196561475

What Socratic 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 Socratic graph.