Evidence mapPaperPMID 40244147Full record

ReviewInternational journal of molecular sciences2025

microRNAs in Type 1 Diabetes: Roles, Pathological Mechanisms, and Therapeutic Potential.

Hayeong Cho, Se Eun Ha, Rajan Singh, David Kim, Seungil Ro

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. 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

5 authors.

Hayeong ChoDepartment of Physiology & Cell Biology, University of Nevada School of Medicine, Reno, NV 89557, USA.ORCID 0000-0003-0594-5153
Se Eun HaDepartment of Physiology & Cell Biology, University of Nevada School of Medicine, Reno, NV 89557, USA.ORCID 0000-0001-6063-5559
Rajan SinghDepartment of Physiology & Cell Biology, University of Nevada School of Medicine, Reno, NV 89557, USA.ORCID 0000-0001-5500-1949
David KimDepartment of Physiology & Cell Biology, University of Nevada School of Medicine, Reno, NV 89557, USA.
Seungil RoDepartment of Physiology & Cell Biology, University of Nevada School of Medicine, Reno, NV 89557, USA.ORCID 0000-0003-0861-8334

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 progressive destruction of pancreatic β-cells, leading to insulin deficiency. The primary drivers of β-cell destruction in T1D involve autoimmune-mediated processes that trigger chronic inflammation and ultimately β-cell loss. Regulatory microRNAs (miRNAs) play a crucial role in modulating these processes by regulating gene expression through post-transcriptional suppression of target mRNAs. Dysregulated miRNAs have been implicated in T1D pathogenesis, serving as both potential diagnostic biomarkers and therapeutic targets. This review explores the role of miRNAs in T1D, highlighting their involvement in disease mechanisms across both rodent models and human patients. While current antidiabetic therapies manage T1D symptoms, they do not prevent β-cell destruction, leaving patients reliant on lifelong insulin therapy. By summarizing key miRNA expression profiles in diabetic animal models and patients, this review explores the potential of miRNA-based therapies to restore β-cell function and halt or slow the progression of the disease.

Indexed as

Diabetes Mellitus, Type 1MicroRNAsAnimalsBiomarkersGene Expression RegulationHumansInsulin-Secreting CellsBiomarkersMicroRNAsapoptosisautoimmune diseasemiRNAstype 1 diabetesβ-cells

Identifiers

PMID40244147
PMCPMC11990060

What Socratic holds

Textmetadata
LicenceCC BY
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.