Evidence map›Paper›PMID 37364817›Full record

ArticleOsteoarthritis and cartilage2023

Red blood cell exposure increases chondrocyte susceptibility to oxidative stress following hemarthrosis.

Andy J Lee, Lianna R Gangi, Fereshteh Zandkarimi, Brent R Stockwell, Clark T Hung

Open access · bronzeAbstract read
In one paragraph

Article in Osteoarthritis and cartilage, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Beyond Killing: The Overlooked Contribution of Neutrophils to Tissue Repair.International journal of molecular sciences · 2025
    Review
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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

5 authors at 1 institution in 1 country.

Andy J LeeDepartment of Biomedical Engineering, Columbia University, 351 Engineering Terrace, Mail Code 8904, 1210 Amsterdam Avenue, New York, NY, USA. Electronic address: jl3924@columbia.edu.
Lianna R GangiDepartment of Biomedical Engineering, Columbia University, 351 Engineering Terrace, Mail Code 8904, 1210 Amsterdam Avenue, New York, NY, USA. Electronic address: lrg2147@columbia.edu.
Fereshteh ZandkarimiDepartment of Chemistry, Columbia University, 216 Havemeyer Hall, 3000 Broadway, Mail Code 3183, New York, NY, USA. Electronic address: fz2262@columbia.edu.
Brent R StockwellDepartment of Chemistry, Columbia University, 216 Havemeyer Hall, 3000 Broadway, Mail Code 3183, New York, NY, USA; Department of Biological Sciences, Columbia University, 1208 NWC Building, 550 West 120th St. M.C. 4846, New York, NY, USA. Electronic address: bstockwell@columbia.edu.
Clark T HungDepartment of Biomedical Engineering, Columbia University, 351 Engineering Terrace, Mail Code 8904, 1210 Amsterdam Avenue, New York, NY, USA; Department of Orthopaedic Surgery, Columbia University, New York, NY, USA. Electronic address: cth6@columbia.edu.
Columbia University · US

Funding

Tissue Engineering Resource Center: TTDP41EB027062 · NIBIB · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Gordana Vunjak-Novakovic · 2019 to 2026
$12.6M
Defining the functions and translational potential of ferroptosisR35CA209896 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI STOCKWELL, BRENT R. · 2016 to 2022
$6.5M
Ferroptosis as a Potential Mechanism of Blood-Induced Chondrocyte Cell DeathF31AR078004 · NIAMS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI LEE, ANDY JAEHAN · 2020 to 2022
$138k
NCI NIH HHS R35 CA209896NIAMS NIH HHS F31 AR078004NIBIB NIH HHS P41 EB027062
6 · The paper itself

Abstract

objectiveThe detrimental effects of blood exposure on articular tissues are well characterized, but the individual contributions of specific whole blood components are yet to be fully elucidated. Better understanding of mechanisms that drive cell and tissue damage in hemophilic arthropathy will inform novel therapeutic strategies. The studies here aimed to identify the specific contributions of intact and lysed red blood cells (RBCs) on cartilage and the therapeutic potential of Ferrostatin-1 in the context of lipid changes, oxidative stress, and ferroptosis.

methodsChanges to biochemical and mechanical properties following intact RBC treatment were assessed in human chondrocyte-based tissue-engineered cartilage constructs and validated against human cartilage explants. Chondrocyte monolayers were assayed for changes to intracellular lipid profiles and the presence of oxidative and ferroptotic mechanisms.

resultsMarkers of tissue breakdown were observed in cartilage constructs without parallel losses in DNA (control: 786.3 (102.2) ng/mg; RBC

conclusionsIntact RBCs induce intracellular phenotypic changes to chondrocytes that increase vulnerability to tissue damage while lysed RBCs have a more direct influence on chondrocyte death by mechanisms that are representative of ferroptosis.

Indexed as

Cartilage, ArticularChondrocytesErythrocytesHemarthrosisHumansLipidsOxidative StressLipidsErythrocyteFerroptosisHemarthrosisHemophilic arthropathyIron

Identifiers

PMID37364817
PMCPMC10529126
OpenAlexW4381953019

What OpenQuestion holds

Textmetadata
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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.