Evidence map›Paper›PMID 29236198›Full record

ArticleApoptosis : an international journal on programmed cell death2018

SDF-1 induces TNF-mediated apoptosis in cardiac myocytes.

Andrew A Jarrah, Martina Schwarskopf, Edward R Wang, Thomas LaRocca, Ashwini Dhume, Shihong Zhang, Lahouria Hadri, Roger J Hajjar, Alison D Schecter, Sima T Tarzami

Open access · greenAbstract read
In one paragraph

Article in Apoptosis : an international journal on programmed cell death, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.7field-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

38 citing papers in PubMed, 51 citations in OpenAlex.

  1. Frontiers in immunology · 2026
    Review
  2. Increased Dipeptidyl Peptidase-4 Promotes Adipose Inflammation and Dysfunction in Mice Under Chronic Stress.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. [Stromal Cell-Derived Factor 1α Inhibits Chondrocyte Apoptosis and Promotes Autophagy Through the Akt Signaling Pathway].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2024
    Article
  7. Review
  8. Review
  9. Article
  10. Extracellular Vesicles and Pathological Cardiac Hypertrophy.Advances in experimental medicine and biology · 2023
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Chemokines in Myocardial Infarction.Journal of cardiovascular translational research · 2021
    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

10 authors at 3 institutions in 1 country.

Andrew A JarrahTufts University School of Medicine, Boston, MA, 02111, USA.
Martina SchwarskopfIcahn School of Medicine at Mount Sinai, Cardiovascular Research Center, New York, NY, 10128, USA.
Edward R WangIcahn School of Medicine at Mount Sinai, Cardiovascular Research Center, New York, NY, 10128, USA.
Thomas LaRoccaIcahn School of Medicine at Mount Sinai, Cardiovascular Research Center, New York, NY, 10128, USA.
Ashwini DhumeIcahn School of Medicine at Mount Sinai, Cardiovascular Research Center, New York, NY, 10128, USA.
Shihong ZhangIcahn School of Medicine at Mount Sinai, Cardiovascular Research Center, New York, NY, 10128, USA.
Lahouria HadriIcahn School of Medicine at Mount Sinai, Cardiovascular Research Center, New York, NY, 10128, USA.
Roger J HajjarIcahn School of Medicine at Mount Sinai, Cardiovascular Research Center, New York, NY, 10128, USA.
Alison D SchecterIcahn School of Medicine at Mount Sinai, Cardiovascular Research Center, New York, NY, 10128, USA.
Sima T TarzamiDepartment of Physiology and Biophysics, Howard University College of Medicine, 520 W Street, NW, Suite 2420, Washington, DC, 20059, USA. sima.tarzami@howard.edu.ORCID 0000-0002-3434-4587
Icahn School of Medicine at Mount Sinai · USHoward University · USTufts University · US

Funding

PROTEOMICS CORE FACILITYG12MD007597 · NIMHD · HOWARD UNIVERSITY · PI SOUTHERLAND, WILLIAM M. · 2012 to 2018
$14.8M
Treating Ventricle and Valve: New Synergies for Ischemic LV Remodeling with MRR01HL128099 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI AKAR, FADI GABRIEL, LEVINE, ROBERT A · 2016 to 2019
$2.8M
Interactions of SERCA2a and BMPRII in Vascular DiseaseR01HL133554 · NHLBI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HADRI, LAHOUARIA · 2016 to 2020
$2.3M
American Heart Association GRNT4180006NHLBI NIH HHS R01 HL128099NHLBI NIH HHS R01 HL133554NIMHD NIH HHS G12 MD007597NIMHD NIH HHS G12MD007597
6 · The paper itself

Abstract

Chemokines are small secreted proteins with chemoattractant properties that play a key role in inflammation. One such chemokine, Stromal cell-derived factor-1 (SDF-1) also known as CXCL12, and its receptor, CXCR4, are expressed and functional in cardiac myocytes. SDF-1 both stimulates and enhances the cellular signal which attracts potentially beneficial stem cells for tissue repair within the ischemic heart. Paradoxically however, this chemokine is known to act in concert with the inflammatory cytokines of the innate immune response which contributes to cellular injury through the recruitment of inflammatory cells during ischemia. In the present study, we have demonstrated that SDF-1 has dose dependent effects on freshly isolated cardiomyocytes. Using Tunnel and caspase 3-activation assays, we have demonstrated that the treatment of isolated adult rat cardiac myocyte with SDF-1 at higher concentrations (pathological concentrations) induced apoptosis. Furthermore, ELISA data demonstrated that the treatment of isolated adult rat cardiac myocyte with SDF-1 at higher concentrations upregulated TNF-α protein expression which directly correlated with subsequent apoptosis. There was a significant reduction in SDF-1 mediated apoptosis when TNF-α expression was neutralized which suggests that SDF-1 mediated apoptosis is TNF-α-dependent. The fact that certain stimuli are capable of driving cardiomyocytes into apoptosis indicates that these cells are susceptible to clinically relevant apoptotic triggers. Our findings suggest that the elevated SDF-1 levels seen in a variety of clinical conditions, including ischemic myocardial infarction, may either directly or indirectly contribute to cardiac cell death via a TNF-α mediated pathway. This highlights the importance of this receptor/ligand in regulating the cardiomyocyte response to stress conditions.

Indexed as

AnimalsApoptosisBenzylaminesCaspase 3Chemokine CXCL12CyclamsDose-Response Relationship, DrugDoxorubicinGene Expression RegulationHeterocyclic CompoundsIsoproterenolMitochondriaMyocytes, CardiacPrimary Cell CultureRatsRats, Sprague-DawleyBenzylaminesCasp3 protein, ratCaspase 3Chemokine CXCL12CXCL12 protein, ratCxcr4 protein, ratCyclamsDoxorubicinHeterocyclic CompoundsIsoproterenolplerixaforReceptors, CXCR4Tumor Necrosis Factor-alphaApoptosisChemokinesStromal derived factor-1 (SDF-1)Tumor necrosis factor (TNF)

Identifiers

PMID29236198
PMCPMC6019273
OpenAlexW2772036482

What OpenQuestion holds

Textmetadata
LicenceTDM
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.