Evidence map›Paper›PMID 33052523›Full record

ReviewReviews in endocrine & metabolic disorders2021

Molecular prospect of type-2 diabetes: Nanotechnology based diagnostics and therapeutic intervention.

Rout George Kerry, Gyana Prakash Mahapatra, Ganesh Kumar Maurya, Sushmita Patra, Subhasis Mahari, Gitishree Das, Jayanta Kumar Patra, Sabuj Sahoo

Abstract readReview
PubMed Publisher
In one paragraph

Review in Reviews in endocrine & metabolic disorders, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Article
  2. Nanotechnology-based biomedical devices in the cancer diagnostics and therapy.Medical oncology (Northwood, London, England) · 2025
    Review
  3. Article
  4. Advances in Nanomedicine for Precision Insulin Delivery.Pharmaceuticals (Basel, Switzerland) · 2024
    Review
  5. Review
  6. Article
  7. Nanotheranostics: application of nanosensors in diabetes management.Journal of diabetes and metabolic disorders · 2023
    Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
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

8 authors.

Rout George KerryDepartment of Biotechnology, Utkal University, Vani Vihar, Bhubaneswar, Odisha, 751004, India.
Gyana Prakash MahapatraMolecular Biophysics Unit, Indian Institute of Science (IISc), Bengaluru, 560012, India.
Ganesh Kumar MauryaZoology Section, Mahila MahaVidyalya, Banaras Hindu University, Varanasi, 221005, India.
Sushmita PatraDepartment of Biotechnology, North Odissa University, Takatpur, Baripada, Odisha, 757003, India.
Subhasis MahariDBT- National Institute of Animal Biotechnology, Hyderabad, 500032, India.
Gitishree DasResearch Institute of Biotechnology & Medical Converged Science, Dongguk University-Seoul, Goyangsi, 10326, Republic of Korea.
Jayanta Kumar PatraResearch Institute of Biotechnology & Medical Converged Science, Dongguk University-Seoul, Goyangsi, 10326, Republic of Korea. jkpatra@dongguk.edu.ORCID 0000-0003-4118-4355
Sabuj SahooDepartment of Biotechnology, Utkal University, Vani Vihar, Bhubaneswar, Odisha, 751004, India. sabujbiotech@utkaluniversity.ac.in.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

About ninety percent of all diabetic conditions account for T2D caused due to abnormal insulin secretion/ action or increased hepatic glucose production. Factors that contribute towards the aetiology of T2D could be well explained through biochemical, molecular, and cellular aspects. In this review, we attempt to explain the recent evolving molecular and cellular advancement associated with T2D pathophysiology. Current progress fabricated in T2D research concerning intracellular signaling cascade, inflammasome, autophagy, genetic and epigenetics changes is discretely explained in simple terms. Present available anti-diabetic therapeutic strategies commercialized and their limitations which are needed to be acknowledged are addressed in the current review. In particular, the pre-eminence of nanotechnology-based approaches to nullify the inadequacy of conventional anti-diabetic therapeutics and heterogeneous nanoparticulated systems exploited in diabetic researches are also discretely mentioned and are also listed in a tabular format in the review. Additionally, as a future prospect of nanotechnology, the review presents several strategic hypotheses to ameliorate the austerity of T2D by an engineered smart targeted nano-delivery system. In detail, an effort has been made to hypothesize novel nanotechnological based therapeutic strategies, which exploits previously described inflammasome, autophagic target points. Utilizing graphical description it is explained how a smart targeted nano-delivery system could promote β-cell growth and development by inducing the Wnt signaling pathway (inhibiting Gsk3β), inhibiting inflammasome (inhibiting NLRP3), and activating autophagic target points (protecting Atg3/Atg7 complex from oxidative stress) thereby might ameliorate the severity of T2D. Additionally, several targeting molecules associated with autophagic and epigenetic factors are also highlighted, which can be exploited in future diabetic research.

Indexed as

Diabetes Mellitus, Type 2Insulin-Secreting CellsHumansInflammasomesNanotechnologyOxidative StressInflammasomesAutophagyEpigeneticsInflammasomeIntracellular signaling cascadeNano-delivery systemsType-2 diabetes

Identifiers

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Registered trials

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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.