Evidence map›Paper›PMID 37035220›Full record

ReviewWorld journal of diabetes2023

Pancreatic β-cell dysfunction in type 2 diabetes: Implications of inflammation and oxidative stress.

Phiwayinkosi V Dludla, Sihle E Mabhida, Khanyisani Ziqubu, Bongani B Nkambule, Sithandiwe E Mazibuko-Mbeje, Sidney Hanser, Albert Kotze Basson, Carmen Pheiffer, Andre Pascal Kengne

Open access · diamondAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in World journal of diabetes, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 165 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
165citing papers in PubMed, 8 pooled it
86.7field-weighted citation impact, top 1% 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

165 citing papers in PubMed, 8 syntheses or guidelines pooled it, 271 citations in OpenAlex.

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  19. Peel of Pomegranate Fruit (Current issues in molecular biology · 2026
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105 more citing papers are in PubMed but not listed here.

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

9 authors at 5 institutions in 1 country.

Phiwayinkosi V DludlaBiomedical Research and Innovation Platform, South African Medical Research Council, Cape Town 7505, South Africa.
Sihle E MabhidaBiomedical Research and Innovation Platform, South African Medical Research Council, Cape Town 7505, South Africa.
Khanyisani ZiqubuDepartment of Biochemistry, North-West University, Mmabatho 2745, South Africa.
Bongani B NkambuleSchool of Laboratory Medicine and Medical Sciences, University of KwaZulu-Natal, Durban 4000, South Africa.
Sithandiwe E Mazibuko-MbejeDepartment of Biochemistry, North-West University, Mmabatho 2745, South Africa.
Sidney HanserDepartment of Physiology and Environmental Health, University of Limpopo, Sovenga 0727, South Africa.
Albert Kotze BassonDepartment of Biochemistry and Microbiology, University of Zululand, KwaDlangezwa 3880, South Africa.
Carmen PheifferBiomedical Research and Innovation Platform, South African Medical Research Council, Cape Town 7505, South Africa.
Andre Pascal KengneDepartment of Medicine, University of Cape Town, Cape Town 7500, South Africa.
South African Medical Research Council · ZANorth-West University · ZAUniversity of KwaZulu-Natal · ZAUniversity of Limpopo · ZAUniversity of Zululand · ZA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin resistance and pancreatic β-cell dysfunction are major pathological mechanisms implicated in the development and progression of type 2 diabetes (T2D). Beyond the detrimental effects of insulin resistance, inflammation and oxidative stress have emerged as critical features of T2D that define β-cell dysfunction. Predominant markers of inflammation such as C-reactive protein, tumor necrosis factor alpha, and interleukin-1β are consistently associated with β-cell failure in preclinical models and in people with T2D. Similarly, important markers of oxidative stress, such as increased reactive oxygen species and depleted intracellular antioxidants, are consistent with pancreatic β-cell damage in conditions of T2D. Such effects illustrate a pathological relationship between an abnormal inflammatory response and generation of oxidative stress during the progression of T2D. The current review explores preclinical and clinical research on the patho-logical implications of inflammation and oxidative stress during the development of β-cell dysfunction in T2D. Moreover, important molecular mechanisms and relevant biomarkers involved in this process are discussed to divulge a pathological link between inflammation and oxidative stress during β-cell failure in T2D. Underpinning the clinical relevance of the review, a systematic analysis of evidence from randomized controlled trials is covered, on the potential therapeutic effects of some commonly used antidiabetic agents in modulating inflammatory makers to improve β-cell function.

Indexed as

InflammationInsulin resistanceOxidative stressType 2 diabetesβ-cell dysfunction

Identifiers

PMID37035220
PMCPMC10075035
OpenAlexW4324381450

What Socratic holds

Textmetadata
LicenceCC BY-NC
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.