Evidence map›Paper›PMID 41805883›Full record

ReviewPLoS pathogens2026

Fifty shades of iron: Unorthodox mechanisms of iron acquisition and utilization in blood-stage Plasmodium parasites.

Kade M Loveridge, Paul A Sigala

Abstract readReview
In one paragraph

Review in PLoS pathogens, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

2 authors.

Kade M LoveridgeDepartment of Biochemistry, University of Utah, Salt Lake City, Utah, United States of America.
Paul A SigalaDepartment of Biochemistry, University of Utah, Salt Lake City, Utah, United States of America.ORCID https://orcid.org/0000-0002-3464-3042

Funding

Function of a putative iron transporter in the Plasmodium apicoplastR21AI185746 · NIAID · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI SIGALA, PAUL A · 2024 to 2025
$424k
NIAID NIH HHS R21 AI185746
6 · The paper itself

Abstract

Plasmodium falciparum parasites cause severe human malaria and depend on iron for essential metabolic processes during all phases of their complicated lifecycle, including when growing in human red blood cells (RBCs). Despite decades of study, the major pathways by which malaria parasites access, distribute, and regulate iron during blood-stage infection remain incompletely defined. The parasite genome lacks many canonical transporters, storage proteins, reductases, and regulatory circuits that are essential for maintaining iron homeostasis in model organisms. Emerging evidence suggests that blood-stage parasites employ unconventional strategies to maintain iron homeostasis. In this review, we synthesize current knowledge of how blood-stage P. falciparum manages iron, from initial uptake through cellular distribution to utilization, highlighting the key proteins and pathways that shape parasite iron metabolism. We also identify major unanswered questions that will guide future efforts to understand and therapeutically target this essential aspect of Plasmodium biology.

Indexed as

ErythrocytesIronMalaria, FalciparumPlasmodium falciparumAnimalsHomeostasisHumansProtozoan ProteinsIronProtozoan Proteins

Identifiers

PMID41805883
PMCPMC12974877

What OpenQuestion 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 OpenQuestion graph.