Cited by 239Erythrocyte Function and PathophysiologyAntioxidant Activity and Oxidative StressCell death mechanisms and regulation

Oxidative stress, eryptosis and anemia: a pivotal mechanistic nexus in systemic diseases

Bissinger, Rosi, Bhuyan, Abdulla Al Mamun, Qadri, Syed M., Lang, Florian·2019·The FEBS Journal

Abstract

The average lifespan of circulating erythrocytes usually exceeds hundred days. Prior to that, however, erythrocytes may be exposed to oxidative stress in the circulation which could cause injury and trigger their suicidal death or eryptosis. Oxidative stress activates Ca 2+ ‐permeable nonselective cation channels in the cell membrane, thus, stimulating Ca 2+ entry and subsequent cell membrane scrambling resulting in phosphatidylserine exposure and activation of Ca 2+ ‐sensitive K + channels leading to K + exit, hyperpolarization, Cl − exit, and ultimately cell shrinkage due to loss of KC l and osmotically driven water. While the mechanistic link between oxidative stress and anemia remains ill‐defined, several diseases such as diabetes, hepatic failure, malignancy, chronic kidney disease and inflammation have been identified to display both increased oxidative stress as well as eryptosis. Recent compelling evidence suggests that oxidative stress is an important perpetrator in accelerating erythrocyte loss in different systemic conditions and an underlying mechanism for anemia associated with these pathological states. In the present review, we discuss the role of oxidative stress in reducing erythrocyte survival and provide novel insights into the possible use of antioxidants as putative antieryptotic and antianemic agents in a variety of systemic diseases.

Integrity signals

Registry

Crossref · 10.1111/febs.14606

Cites

290 of 290 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • The life-span of RBC can be pathologically reduced in hemolytic anemias such as G6PD deficiency, or when chronic kidney disease or inflammation cause premature erythrocyte decay, named eryptosis.

    “The life-span of RBC can be pathologically reduced in hemolytic anemias, such as G6PD deficiency, or when chronic kidney disease or inflammation cause premature erythrocyte decay, named eryptosis (Bissinger et al., 2018).”

    From Iron in infection and immunity (2020) · cites this paper as Bissinger et al., 2018

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Bissinger, R., Bhuyan, A. A. M., Qadri, S. M., & Lang, F.
Affiliations
  • University of Tübingen (DE)
  • Canadian Blood Services (CA)
  • Heinrich Heine University Düsseldorf (DE)
Corresponding author
Bissinger, Rosi
Venue
The FEBS Journal
Publisher
Wiley
Published
2018-08-18
Volume
286
Issue
5
Pages
826-854
ISSN
  • 1742-464X (ISSN-L)
  • 1742-4658
OpenAlex
W2883478372
Cited by
239
References
290
Citations by year
2026: 29 · 2025: 35 · 2024: 33 · 2023: 33 · 2022: 37 · 2021: 37 · 2020: 20 · 2019: 11 · 2018: 3
FWCI
2.33
Type
journal article
Language
en
Open access
closed
Locations
  • FEBS Journal (publishedVersion)
  • PubMed (publishedVersion)
Funders
Deutsche Forschungsgemeinschaft
Topics
  • Health Sciences › Medicine › Physiology › Erythrocyte Function and Pathophysiology
  • Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords
oxidative stress, eryptosis, anemia, erythrocyte survival, erythrocyte death, calcium-permeable cation channel, phosphatidylserine exposure, potassium channels, antioxidants, diabetes mellitus, chronic kidney disease, inflammation, liver failure, cancer
MeSH terms
Eryptosis, Anemia, Animals, Erythrocytes, Hematologic Diseases, Humans, Ion Channels, Signal Transduction, Ion Transport, Oxidative Stress

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review