Evidence map›Paper›PMID 35492364›Full record

SynthesisFrontiers in medicine2022

New Insights Into Pathophysiology of β-Thalassemia.

Maria Sanchez-Villalobos, Miguel Blanquer, Jose M Moraleda, Eduardo J Salido, Ana B Perez-Oliva

Open access · goldAbstract readSystematic Review
In one paragraph

Synthesis in Frontiers in medicine, 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
6.9field-weighted citation impact, top 2% 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, 47 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Beta thalassemia syndromes: New insights.World journal of clinical cases · 2025
    Review
  16. Cardiac Dysfunction in β-Thalassemia: A Narrative Review.Research in heart yield and translational medicine · 2025
    Review
  17. Whole Blood Transcriptome Analysis in Congenital Anemia Patients.International journal of molecular sciences · 2024
    Article
  18. Article
  19. Article
  20. 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 2 institutions in 1 country.

Maria Sanchez-VillalobosHematology Service, Virgen de la Arrixaca University Hospital, Murcia, Spain.
Miguel BlanquerHematology Service, Virgen de la Arrixaca University Hospital, Murcia, Spain.
Jose M MoraledaHematology Service, Virgen de la Arrixaca University Hospital, Murcia, Spain.
Eduardo J SalidoHematology Service, Virgen de la Arrixaca University Hospital, Murcia, Spain.
Ana B Perez-OlivaBiomedical Research Institute of Murcia (IMIB), Murcia, Spain.
Instituto Murciano de Investigación Biosanitaria · ESHospital Universitario Virgen de la Arrixaca · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

β-thalassemia is a disease caused by genetic mutations including a nucleotide change, small insertions or deletions in the β-globin gene, or in rare cases, gross deletions into the β-globin gene. These mutations affect globin-chain subunits within the hemoglobin tetramer what induces an imbalance in the α/β-globin chain ratio, with an excess of free α-globin chains that triggers the most important pathogenic events of the disease: ineffective erythropoiesis, chronic anemia/chronic hypoxia, compensatory hemopoietic expansion and iron overload. Based on advances in our knowledge of the pathophysiology of β-thalassemia, in recent years, emerging therapies and clinical trials are being conducted and are classified into three major categories based on the different approach features of the underlying pathophysiology: correction of the α/β-globin disregulation; improving iron overload and reverse ineffective erythropoiesis. However, pathways such as the dysregulation of transcriptional factors, activation of the inflammasome, or approach to mechanisms of bone mineral loss, remain unexplored for future therapeutic targets. In this review, we update the main pathophysiological pathways involved in β-thalassemia, focusing on the development of new therapies directed at new therapeutic targets.

Indexed as

anemiaGATA1inflammasomethalassemiaβ-globin

Identifiers

PMID35492364
PMCPMC9041707
OpenAlexW4223442589

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.