Evidence map›Paper›PMID 34831062›Full record

ReviewCells2021

Iron Metabolism in Pancreatic Beta-Cell Function and Dysfunction.

Algerta Marku, Alessandra Galli, Paola Marciani, Nevia Dule, Carla Perego, Michela Castagna

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
5.7field-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

40 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
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  4. Mitochondria-associated programmed cell death in pancreatic β cell of T2DM.Apoptosis : an international journal on programmed cell death · 2026
    Review
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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

6 authors at 1 institution in 1 country.

Algerta MarkuDepartment of Excellence Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Via Trentacoste, 22134 Milano, Italy.
Alessandra GalliDepartment of Excellence Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Via Trentacoste, 22134 Milano, Italy.ORCID 0000-0001-9023-1571
Paola MarcianiDepartment of Excellence Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Via Trentacoste, 22134 Milano, Italy.ORCID 0000-0001-6812-1384
Nevia DuleDepartment of Excellence Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Via Trentacoste, 22134 Milano, Italy.
Carla PeregoDepartment of Excellence Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Via Trentacoste, 22134 Milano, Italy.ORCID 0000-0003-3027-1779
Michela CastagnaDepartment of Excellence Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Via Trentacoste, 22134 Milano, Italy.ORCID 0000-0001-8144-9173
University of Milan · IT

Funding

MIUR Progetto Dipartimenti di Eccellenza. N.D. is supported by Università degli Studi di Milano (Ph.D. fellowship)Regione Lombardia Bando F&S Aggregazioni POR FESR 2014-2020
6 · The paper itself

Abstract

Iron is an essential element involved in a variety of physiological functions. In the pancreatic beta-cells, being part of Fe-S cluster proteins, it is necessary for the correct insulin synthesis and processing. In the mitochondria, as a component of the respiratory chain, it allows the production of ATP and reactive oxygen species (ROS) that trigger beta-cell depolarization and potentiate the calcium-dependent insulin release. Iron cellular content must be finely tuned to ensure the normal supply but also to prevent overloading. Indeed, due to the high reactivity with oxygen and the formation of free radicals, iron excess may cause oxidative damage of cells that are extremely vulnerable to this condition because the normal elevated ROS production and the paucity in antioxidant enzyme activities. The aim of the present review is to provide insights into the mechanisms responsible for iron homeostasis in beta-cells, describing how alteration of these processes has been related to beta-cell damage and failure. Defects in iron-storing or -chaperoning proteins have been detected in diabetic conditions; therefore, the control of iron metabolism in these cells deserves further investigation as a promising target for the development of new disease treatments.

Indexed as

AnimalsDiabetes MellitusHomeostasisHumansInsulin-Secreting CellsIronModels, BiologicalIronbeta-cell functiondiabetesIron metabolismreactive oxygen species

Identifiers

PMID34831062
PMCPMC8616520
OpenAlexW3209794245

What OpenQuestion 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 OpenQuestion graph.