Hereditary hemochromatosis with homozygous C282Y HFE mutation: possible clinical model to assess effects of elevated reactive oxygen species on the development of cardiovascular disease.

Yukitaka Shizukuda, Douglas R Rosing

Abstract readReview

In one paragraph

Review in Molecular and cellular biochemistry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it

0cells of the map it votes in

0citing papers in PubMed

0.3field-weighted citation impact, top 38% of its field

1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

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0 citing papers in PubMed, 1 citations in OpenAlex.

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4 · The record

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5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Yukitaka ShizukudaCardiovascular Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, 20892, USA. shizukya@ucmail.uc.edu.

Douglas R RosingCardiovascular Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, 20892, USA.

Cincinnati VA Medical Center · USNational Institutes of Health · US

Funding

NHLBI NIH HHS Intramural 00000

6 · The paper itself

Abstract

Hereditary hemochromatosis with the homozygous C282Y HFE mutation (HH-282H) is a genetic condition which causes iron overload (IO) and elevated reactive oxygen species (ROS) secondary to the IO. Interestingly, even after successful iron removal therapy, HH-282H subjects demonstrate chronically elevated ROS. Raised ROS are also associated with the development of multiple cardiovascular diseases and HH-282H subjects may be at risk to develop these complications. In this narrative review, we consider HH-282H subjects as a clinical model for assessing the contribution of elevated ROS to the development of cardiovascular diseases in subjects with fewer confounding clinical risk factors as compared to other disease conditions with high ROS. We identify HH-282H subjects as a potentially unique clinical model to assess the impact of chronically elevated ROS on the development of cardiovascular disease and to serve as a clinical model to detect effective interventions for anti-ROS therapy.

Indexed as

Cardiovascular DiseasesHemochromatosisHemochromatosis ProteinIron OverloadHistocompatibility Antigens Class IHumansMembrane ProteinsMutationReactive Oxygen SpeciesHemochromatosis ProteinHFE protein, humanHistocompatibility Antigens Class IMembrane ProteinsReactive Oxygen SpeciesCardiovascular diseaseClinical modelHereditary hemochromatosisIron overloadOxidative stressReactive oxygen species

Identifiers

PMID37133674

DOI10.1007/s11010-023-04726-y

OpenAlexW4367834208

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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.