Evidence map›Paper›PMID 39207733›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2024

Lysis of human erythrocytes due to Piezo1-dependent cytosolic calcium overload as a mechanism of circulatory removal.

Lennart Kuck, Antony P McNamee, Maria Bordukova, Ario Sadafi, Carsten Marr, Jason N Peart, Michael J Simmonds

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

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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

7 authors.

Lennart KuckBiorheology Research Laboratory, Griffith University, QLD 4215, Australia.
Antony P McNameeBiorheology Research Laboratory, Griffith University, QLD 4215, Australia.ORCID 0000-0002-4473-487X
Maria BordukovaInstitute of Computational Biology, Computational Health Center, Helmholtz Munich, Munich 85764, Germany.ORCID 0009-0008-0956-5506
Ario SadafiInstitute of AI for Health, Helmholtz Zentrum München-German Research Center for Environmental Health, Neuherberg 85764, Germany.
Carsten MarrInstitute of AI for Health, Helmholtz Zentrum München-German Research Center for Environmental Health, Neuherberg 85764, Germany.ORCID 0000-0003-2154-4552
Jason N PeartSchool of Pharmacy and Medical Sciences, Griffith University Gold Coast, QLD 4215, Australia.
Michael J SimmondsBiorheology Research Laboratory, Griffith University, QLD 4215, Australia.ORCID 0000-0001-8145-6787

Funding

Australian Research Council DE240100236Australian Research Council DP230100556European Union’s Horizon 2020 Research and Innovation Program 866411Medical Research Future RFRHPI000241
6 · The paper itself

Abstract

Hematopoietic stem cells surrender organelles during differentiation, leaving mature red blood cells (RBC) devoid of transcriptional machinery and mitochondria. The resultant absence of cellular repair capacity limits RBC circulatory longevity, and old cells are removed from circulation. The specific age-dependent alterations required for this apparently targeted removal of RBC, however, remain elusive. Here, we assessed the function of Piezo1, a stretch-activated transmembrane cation channel, within subpopulations of RBC isolated based on physical properties associated with aging. We subsequently investigated the potential role of Piezo1 in RBC removal, using pharmacological and mechanobiological approaches. Dense (old) RBC were separated from whole blood using differential density centrifugation. Tolerance of RBC to mechanical forces within the physiological range was assessed on single-cell and cell population levels. Expression and function of Piezo1 were investigated in separated RBC populations by monitoring accumulation of cytosolic Ca

Indexed as

CalciumCytosolErythrocytesIon ChannelsHemolysisHumansCalciumIon ChannelsPIEZO1 protein, humancalcium signalinghemolysismechanotransductionPiezo1red blood cells

Identifiers

PMID39207733
PMCPMC11388408

What OpenQuestion holds

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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.