Evidence map›Paper›PMID 35806451›Full record

ReviewInternational journal of molecular sciences2022

Metabolic Reprogramming in Sickle Cell Diseases: Pathophysiology and Drug Discovery Opportunities.

Dina Alramadhani, Anfal S Aljahdali, Osheiza Abdulmalik, B Daniel Pierce, Martin K Safo

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

7 citing papers in PubMed, 8 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Review
  5. Whole Blood Transcriptome Analysis in Congenital Anemia Patients.International journal of molecular sciences · 2024
    Article
  6. Article
  7. Review
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

5 authors at 4 institutions in 2 countries.

Dina AlramadhaniDepartment of Medicinal Chemistry and the Institute for Structural Biology, Drug Discovery and Development, School of Pharmacy, Virginia Commonwealth University, Richmond, VA 23298, USA.
Anfal S AljahdaliDepartment of Pharmaceutical Chemistry, King Abdulaziz University, Alsulaymanyah, Jeddah 21589, Saudi Arabia.
Osheiza AbdulmalikDivision of Hematology, The Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA.ORCID 0000-0003-2497-4291
B Daniel PierceDepartment of Biology, University of Richmond, Richmond, VA 23173, USA.
Martin K SafoDepartment of Medicinal Chemistry and the Institute for Structural Biology, Drug Discovery and Development, School of Pharmacy, Virginia Commonwealth University, Richmond, VA 23298, USA.ORCID 0000-0002-9536-1743
Virginia Commonwealth University · USChildren's Hospital of Philadelphia · USKing Abdulaziz University · SAUniversity of Richmond · US

Funding

Targeted Identification of Dual Acting Antisickling Agents for Sickle Cell Disease TherapyR61HL156158 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI ABDULMALIK, OSHEIZA Y, SAFO, MARTIN K · 2021 to 2022
$1.1M
Targeted Identification of Dual Acting Antisickling Agents for Sickle Cell Disease TherapyR33HL156158 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI ABDULMALIK, OSHEIZA Y, SAFO, MARTIN K · 2023 to 2023
$572k
NHLBI NIH HHS R33 HL156158NHLBI NIH HHS R61 HL156158NIH HHS R61HL156158
6 · The paper itself

Abstract

Sickle cell disease (SCD) is a genetic disorder that affects millions of individuals worldwide. Chronic anemia, hemolysis, and vasculopathy are associated with SCD, and their role has been well characterized. These symptoms stem from hemoglobin (Hb) polymerization, which is the primary event in the molecular pathogenesis of SCD and contributes to erythrocyte or red blood cell (RBC) sickling, stiffness, and vaso-occlusion. The disease is caused by a mutation at the sixth position of the β-globin gene, coding for sickle Hb (HbS) instead of normal adult Hb (HbA), which under hypoxic conditions polymerizes into rigid fibers to distort the shapes of the RBCs. Only a few therapies are available, with the universal effectiveness of recently approved therapies still being monitored. In this review, we first focus on how sickle RBCs have altered metabolism and then highlight how this understanding reveals potential targets involved in the pathogenesis of the disease, which can be leveraged to create novel therapeutics for SCD.

Indexed as

Anemia, Sickle CellVascular DiseasesDrug DiscoveryErythrocytes, AbnormalHemoglobin AHemoglobin, SickleHumansHemoglobin AHemoglobin, Sickle2,3-biphosphoglyceratebisphosphoglycerate mutaseEmbden–Meyerhof–Parnas pathwayglucose-6-phosphate dehydrogenaseglyceraldehyde-3-phosphate dehydrogenaseglycolysispentose phosphate pathwaypyruvate kinasesickle cell diseasetriosephosphate isomerase

Identifiers

PMID35806451
PMCPMC9266828
OpenAlexW4283801890

What Socratic 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 Socratic graph.