Evidence map›Paper›PMID 41685625›Full record

ReviewCell transplantation

Advances in stem cell-derived beta-cell therapy: A new frontier in type 1 diabetes treatment.

Krishnaa Shivkant Upadhye, Paritosh Tayade

Abstract readReview
In one paragraph

Review in Cell transplantation. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. 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

2 authors.

Krishnaa Shivkant UpadhyeClinical Pharmacology & Drug Development, Krescent Medical Research Pvt. Ltd., Pune, India.ORCID 0009-0005-9805-7914
Paritosh TayadeClinical Pharmacology & Drug Development, Krescent Medical Research Pvt. Ltd., Pune, India.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 1 diabetes (T1D) is a chronic autoimmune disease characterized by the destruction of pancreatic beta cells (β-cell), leading to lifelong dependence on exogenous insulin. Despite advances in insulin delivery systems and glucose monitoring, achieving tight glycemic control remains a challenge for many patients. In recent years, stem cell-derived β-cell therapy has emerged as a promising strategy for restoring endogenous insulin production. This review explores the progress in differentiating human pluripotent stem cells, such as embryonic stem cells and induced pluripotent stem cells (iPSCs), into functional insulin-secreting β-like cells. We highlight recent breakthroughs in improving cell maturity, graft survival, and immune protection. Delivery approaches, encapsulation technologies, and transplantation strategies are discussed alongside an overview of ongoing clinical trials. The review also addresses current limitations, including immune rejection, cell dedifferentiation, and safety concerns. Finally, we examine future directions, such as genome editing, personalized cell therapy, and the integration of artificial intelligence in monitoring and optimizing treatment. Stem cell-derived β-cell therapy holds transformative potential as a curative approach for T1D, but further research is essential to overcome remaining barriers to its widespread clinical application.

Indexed as

Cell- and Tissue-Based TherapyDiabetes Mellitus, Type 1Insulin-Secreting CellsStem Cell TransplantationAnimalsCell DifferentiationEmbryonic Stem CellsHumansInduced Pluripotent Stem Cellsclinical trialsimmune evasioninduced pluripotent stem cellsislet transplantationregenerative medicinestem cellsType 1 diabetesβ-cell replacement

Identifiers

PMID41685625
PMCPMC12905087

What OpenQuestion holds

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LicenceCC BY-NC
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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.