Evidence map›Paper›PMID 36358555›Full record

ReviewAntioxidants (Basel, Switzerland)2022

Mutual Regulation between Redox and Hypoxia-Inducible Factors in Cardiovascular and Renal Complications of Diabetes.

Carla Iacobini, Martina Vitale, Jonida Haxhi, Carlo Pesce, Giuseppe Pugliese, Stefano Menini

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

Review in Antioxidants (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 2 pooled it
3.2field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 2 syntheses or guidelines pooled it, 36 citations in OpenAlex.

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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 2 institutions in 1 country.

Carla IacobiniDepartment of Clinical and Molecular Medicine, "La Sapienza" University, 00189 Rome, Italy.ORCID 0000-0002-0737-1213
Martina VitaleDepartment of Clinical and Molecular Medicine, "La Sapienza" University, 00189 Rome, Italy.ORCID 0000-0003-4856-7279
Jonida HaxhiDepartment of Clinical and Molecular Medicine, "La Sapienza" University, 00189 Rome, Italy.ORCID 0000-0003-2319-869X
Carlo PesceDepartment of Neurosciences, Rehabilitation, Ophthalmology, Genetic and Maternal Infantile Sciences (DINOGMI), Department of Excellence of MIUR, University of Genoa Medical School, 16132 Genoa, Italy.
Giuseppe PuglieseDepartment of Clinical and Molecular Medicine, "La Sapienza" University, 00189 Rome, Italy.ORCID 0000-0003-1574-0397
Stefano MeniniDepartment of Clinical and Molecular Medicine, "La Sapienza" University, 00189 Rome, Italy.ORCID 0000-0001-7328-2385
Sapienza University of Rome · ITUniversity of Genoa · IT

Funding

European Foundation for the Study of Diabetes (EFSD) and Sanofi EFSD European Research Programme in Macrovascular Complications of Diabetes 2019Sapienza University of Rome "Progetti di Ateneo" 2017, 2020, and 2021
6 · The paper itself

Abstract

Oxidative stress and hypoxia-inducible factors (HIFs) have been implicated in the pathogenesis of diabetic cardiovascular and renal diseases. Reactive oxygen species (ROS) mediate physiological and pathophysiological processes, being involved in the modulation of cell signaling, differentiation, and survival, but also in cyto- and genotoxic damage. As master regulators of glycolytic metabolism and oxygen homeostasis, HIFs have been largely studied for their role in cell survival in hypoxic conditions. However, in addition to hypoxia, other stimuli can regulate HIFs stability and transcriptional activity, even in normoxic conditions. Among these, a regulatory role of ROS and their byproducts on HIFs, particularly the HIF-1α isoform, has received growing attention in recent years. On the other hand, HIF-1α and HIF-2α exert mutually antagonistic effects on oxidative damage. In diabetes, redox-mediated HIF-1α deregulation contributes to the onset and progression of cardiovascular and renal complications, and recent findings suggest that deranged HIF signaling induced by hyperglycemia and other cellular stressors associated with metabolic disorders may cause mitochondrial dysfunction, oxidative stress, and inflammation. Understanding the mechanisms of mutual regulation between HIFs and redox factors and the specific contribution of the two main isoforms of HIF-α is fundamental to identify new therapeutic targets for vascular complications of diabetes.

Indexed as

advanced glycation end productsatherosclerosisdiabetic kidney diseaseinflammationmethylglyoxalprolyl hydroxylase domain proteinsreactive oxygen speciessirtuin-1sodium glucose co-transporter 2 inhibitorsWarburg effect

Identifiers

PMID36358555
PMCPMC9686572
OpenAlexW4308334100

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.