Evidence map›Paper›PMID 36769414›Full record

ReviewJournal of clinical medicine2023

Mitochondria: Emerging Consequential in Sickle Cell Disease.

Mohammad S Akhter, Hassan A Hamali, Hina Rashid, Gasim Dobie, Aymen M Madkhali, Abdullah A Mobarki, Johannes Oldenburg, Arijit Biswas

Abstract readReview
In one paragraph

Review in Journal of clinical medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
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

10 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
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

8 authors.

Mohammad S AkhterDepartment of Medical Laboratory Technology, College of Applied Medical Sciences, Jazan University, Jizan 45142, Saudi Arabia.
Hassan A HamaliDepartment of Medical Laboratory Technology, College of Applied Medical Sciences, Jazan University, Jizan 45142, Saudi Arabia.ORCID 0000-0003-3791-460X
Hina RashidDepartment of Pharmacology and Toxicology, College of Pharmacy, Jazan University, Jizan 45142, Saudi Arabia.
Gasim DobieDepartment of Medical Laboratory Technology, College of Applied Medical Sciences, Jazan University, Jizan 45142, Saudi Arabia.ORCID 0000-0002-9225-1709
Aymen M MadkhaliDepartment of Medical Laboratory Technology, College of Applied Medical Sciences, Jazan University, Jizan 45142, Saudi Arabia.ORCID 0000-0002-0048-4071
Abdullah A MobarkiDepartment of Medical Laboratory Technology, College of Applied Medical Sciences, Jazan University, Jizan 45142, Saudi Arabia.
Johannes OldenburgInstitute of Experimental Haematology and Transfusion Medicine, University Clinic Bonn, 53127 Bonn, Germany.ORCID 0000-0002-1585-4100
Arijit BiswasInstitute of Experimental Haematology and Transfusion Medicine, University Clinic Bonn, 53127 Bonn, Germany.ORCID 0000-0002-4103-5854

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Advanced mitochondrial multi-omics indicate a multi-facet involvement of mitochondria in the physiology of the cell, changing the perception of mitochondria from being just the energy-generating organelles to organelles that highly influence cell structure, function, signaling, and cell fate. This sets mitochondrial dysfunction in the centerstage of numerous acquired and genetic diseases. Sickle cell disease is also being increasingly associated with mitochondrial anomalies and the pathophysiology of sickle cell disease finds mitochondria at crucial intersections in the pathological cascade. Altered mitophagy, increased ROS, and mitochondrial DNA all contribute to the condition and its severity. Such mitochondrial aberrations lead to consequent mitochondrial retention in red blood cells in sickle cell diseases, increased oxidation in the cellular environment, inflammation, worsened vaso-occlusive crisis, etc. There are increasing studies indicating mitochondrial significance in sickle cell disease, consequently providing an opportunity to target it for improving the outcomes of treatment. Identification of the impaired mitochondrial attributes in sickle cell disease and their modulation by therapeutic interventions can impart a better management of the disease. This review aims to describe the mitochondria in the perspective of sicke cell disease so as to provide the reader an overview of the emerging mitochondrial stance in sickle cell disease.

Indexed as

mitochondriamitochondrial retentionmtDNAROSsickle cell disease

Identifiers

PMID36769414
PMCPMC9917941

What OpenQuestion holds

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Registered trials

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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.