Evidence map›Paper›PMID 33125066›Full record

ArticleCardiovascular research2022

Selectin-targeting glycosaminoglycan-peptide conjugate limits neutrophil-mediated cardiac reperfusion injury.

Tima Dehghani, Phung N Thai, Harkanwalpreet Sodhi, Lu Ren, Padmini Sirish, Carol E Nader, Valeriy Timofeyev, James L Overton, Xiaocen Li, Kit S Lam and 2 more

Open access · greenAbstract read
In one paragraph

Article in Cardiovascular research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

15 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Biomimetic strategies for the deputization of proteoglycan functions.Frontiers in cell and developmental biology · 2024
    Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Proteoglycans and proteoglycan mimetics for tissue engineering.American journal of physiology. Cell physiology · 2022
    Review
  12. Review
  13. Review
  14. Review
  15. Article
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

12 authors at 2 institutions in 1 country.

Tima DehghaniDepartment of Biomedical Engineering, University of California, 451 Health Sciences Drive, GBSF 2303, Davis, CA 95616, USA.ORCID 0000-0001-7563-2668
Phung N ThaiDepartment of Internal Medicine, Division of Cardiovascular Medicine, University of California, Davis, CA, USA.ORCID 0000-0001-7344-150X
Harkanwalpreet SodhiDepartment of Biomedical Engineering, University of California, 451 Health Sciences Drive, GBSF 2303, Davis, CA 95616, USA.ORCID 0000-0003-4614-503X
Lu RenDepartment of Internal Medicine, Division of Cardiovascular Medicine, University of California, Davis, CA, USA.ORCID 0000-0002-9731-8562
Padmini SirishDepartment of Internal Medicine, Division of Cardiovascular Medicine, University of California, Davis, CA, USA.
Carol E NaderDepartment of Internal Medicine, Division of Cardiovascular Medicine, University of California, Davis, CA, USA.
Valeriy TimofeyevDepartment of Internal Medicine, Division of Cardiovascular Medicine, University of California, Davis, CA, USA.
James L OvertonDepartment of Internal Medicine, Division of Cardiovascular Medicine, University of California, Davis, CA, USA.ORCID 0000-0002-6527-1763
Xiaocen LiDepartment of Biochemistry and Molecular Medicine, University of California, Davis, CA, USA.
Kit S LamDepartment of Biochemistry and Molecular Medicine, University of California, Davis, CA, USA.
Nipavan ChiamvimonvatDepartment of Internal Medicine, Division of Cardiovascular Medicine, University of California, Davis, CA, USA.
Alyssa PanitchDepartment of Biomedical Engineering, University of California, 451 Health Sciences Drive, GBSF 2303, Davis, CA 95616, USA.ORCID 0000-0002-0360-1480
University of California, Davis · USVA Northern California Health Care System · US

Funding

Staff InvestigatorsP30CA093373 · NCI · UNIVERSITY OF CALIFORNIA DAVIS · PI Gina M Dayton · 2002 to 2026
$84.9M
Functional Interactions of Cardiac Ion ChannelsR01HL085844 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHIAMVIMONVAT, NIPAVAN · 2007 to 2025
$7.3M
Training Program In Basic & Translational Cardiovascular ScienceT32HL086350 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Martin Cadeiras, David A. Liem · 2008 to 2026
$7.1M
Translational Study of Cardiac DysfunctionR01HL085727 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHIAMVIMONVAT, NIPAVAN, SIRISH, PADMINI · 2008 to 2022
$5.7M
Decoding the enigma of cardiac amplificationR01HL137228 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHIAMVIMONVAT, NIPAVAN · 2017 to 2020
$2.2M
Novel Mechanisms of Cardiac pH Regulation During Ischemia/ReperfusionF32HL149288 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI THAI, PHUNG NHAT · 2019 to 2020
$91k
Metabolomics study in patients post myocardial infarctionI01CX001490 · VA · VA NORTHERN CALIFORNIA HEALTH CARE SYS · PI CHIAMVIMONVAT, NIPAVAN · 2017 to 2021
–
Regulation of ion channels in the heartI01BX000576 · VA · VA NORTHERN CALIFORNIA HEALTH CARE SYS · PI CHIAMVIMONVAT, NIPAVAN · 2009 to 2019
–
BLRD VA I01 BX000576CSRD VA I01 CX001490NCI NIH HHS P30 CA093373NHLBI NIH HHS F32 HL149288NHLBI NIH HHS R01 HL085727NHLBI NIH HHS R01 HL085844NHLBI NIH HHS R01 HL137228NHLBI NIH HHS S10 RR033106NHLBI NIH HHS T32 HL086350
6 · The paper itself

Abstract

aimsOne of the hallmarks of myocardial infarction (MI) is excessive inflammation. During an inflammatory insult, damaged endothelial cells shed their glycocalyx, a carbohydrate-rich layer on the cell surface which provides a regulatory interface to immune cell adhesion. Selectin-mediated neutrophilia occurs as a result of endothelial injury and inflammation. We recently designed a novel selectin-targeting glycocalyx mimetic (termed DS-IkL) capable of binding inflamed endothelial cells. This study examines the capacity of DS-IkL to limit neutrophil binding and platelet activation on inflamed endothelial cells, as well as the cardioprotective effects of DS-IkL after acute myocardial infarction. METHODS AND

resultsIn vitro, DS-IkL diminished neutrophil interactions with both recombinant selectin and inflamed endothelial cells, and limited platelet activation on inflamed endothelial cells. Our data demonstrated that DS-IkL localized to regions of vascular inflammation in vivo after 45 min of left anterior descending coronary artery ligation-induced MI. Further, findings from this study show DS-IkL treatment had short- and long-term cardioprotective effects after ischaemia/reperfusion of the left anterior descending coronary artery. Mice treated with DS-IkL immediately after ischaemia/reperfusion and 24 h later exhibited reduced neutrophil extravasation, macrophage accumulation, fibroblast and endothelial cell proliferation, and fibrosis compared to saline controls.

conclusionsOur findings suggest that DS-IkL has great therapeutic potential after MI by limiting reperfusion injury induced by the immune response.

Indexed as

AnimalsAnti-Inflammatory AgentsCell AdhesionCell ProliferationCells, CulturedDisease Models, AnimalEndothelial CellsE-SelectinFemaleFibrosisHumansMaleMiceMice, Inbred C57BLMyocardial InfarctionMyocardial Reperfusion InjuryAnti-Inflammatory AgentsE-SelectinEndothelial cell dysfunctionFibrosisGlycocalyxInflammationMyocardial infarction

Identifiers

PMID33125066
PMCPMC8932156
OpenAlexW3097753642

What OpenQuestion holds

Textmetadata
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.