Evidence map›Paper›PMID 27650096›Full record

ReviewAntioxidants & redox signaling2017

HbE/β-Thalassemia and Oxidative Stress: The Key to Pathophysiological Mechanisms and Novel Therapeutics.

Rhoda Elison Hirsch, Nathawut Sibmooh, Suthat Fucharoen, Joel M Friedman

Open access · greenAbstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% 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, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

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  3. Salivary biomarkers and their association with dental caries and oral health status in children with β-thalassaemia: a case-control study.European archives of paediatric dentistry : official journal of the European Academy of Paediatric Dentistry · 2026
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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

4 authors at 2 institutions in 2 countries.

Rhoda Elison Hirsch1 Department of Medicine (Hematology), Albert Einstein College of Medicine , Bronx, New York.
Nathawut Sibmooh3 Department of Pharmacology, Faculty of Science, Mahidol University , Bangkok, Thailand .
Suthat Fucharoen4 Thalassemia Research Center, Institute of Molecular Biosciences, Mahidol University , Nakornpathom, Thailand .
Joel M Friedman5 Department of Physiology and Biophysics, Albert Einstein College of Medicine , Bronx, New York.
Albert Einstein College of Medicine · USMahidol University · TH

Funding

Recombinant HbAp Production for In Vivo Toxicity StudiesP01HL110900 · NHLBI · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI FRIEDMAN, JOEL M · 2012 to 2016
$10.6M
Production of Bioactive NO: Origin of Hemoglobin E Associated PathophysiologyR21HL106421 · NHLBI · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI FRIEDMAN, JOEL M, HIRSCH, RHODA · 2011 to 2012
$457k
NHLBI NIH HHS P01 HL110900NHLBI NIH HHS R21 HL106421
6 · The paper itself

Abstract

significanceOxidative stress and generation of free radicals are fundamental in initiating pathophysiological mechanisms leading to an inflammatory cascade resulting in high rates of morbidity and death from many inherited point mutation-derived hemoglobinopathies. Hemoglobin (Hb)E is the most common point mutation worldwide. The β CRITICAL ISSUES: While HbE by itself presents as a mild anemia and a single gene for β-thalassemia is not serious, it remains unexplained why HbE/β-thalassemia (HbE/β-thal) is a grave disease with high morbidity and mortality. Patients often exhibit defective physical development, severe chronic anemia, and often die of cardiovascular disease and severe infections. Recent Advances: This article presents an overview of HbE/β-thal disease with an emphasis on new findings pointing to pathophysiological mechanisms derived from and initiated by the dysfunctional property of HbE as a reduced nitrite reductase concomitant with excess α-chains exacerbating unstable HbE, leading to a combination of nitric oxide imbalance, oxidative stress, and proinflammatory events. FUTURE DIRECTIONS: Additionally, we present new therapeutic strategies that are based on the emerging molecular-level understanding of the pathophysiology of this and other hemoglobinopathies. These strategies are designed to short-circuit the inflammatory cascade leading to devastating chronic morbidity and fatal consequences. Antioxid. Redox Signal. 26, 794-813.

Indexed as

Oxidative StressAnimalsbeta-ThalassemiaHemoglobin EHemoglobinopathiesHumansPoint MutationHemoglobin Ehemoglobin Ehypoxiainflammationnitric oxideoxidative stressβ-thalassemia

Identifiers

PMID27650096
PMCPMC5421591
OpenAlexW2557351719

What OpenQuestion holds

Textmetadata
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.