Video: Every Case Tells a Story| Webinar: ACR/CHEST ILD Guidelines in Practice

An official publication of the ACR and the ARP serving rheumatologists and rheumatology professionals

  • Conditions
    • Axial Spondyloarthritis
    • Gout and Crystalline Arthritis
    • Myositis
    • Osteoarthritis and Bone Disorders
    • Pain Syndromes
    • Pediatric Conditions
    • Psoriatic Arthritis
    • Rheumatoid Arthritis
    • Sjögren’s Disease
    • Systemic Lupus Erythematosus
    • Systemic Sclerosis
    • Vasculitis
    • Other Rheumatic Conditions
  • FocusRheum
    • ANCA-Associated Vasculitis
    • Axial Spondyloarthritis
    • Gout
    • Psoriatic Arthritis
    • Rheumatoid Arthritis
    • Systemic Lupus Erythematosus
  • Guidance
    • Clinical Criteria/Guidelines
    • Ethics
    • Legal Updates
    • Legislation & Advocacy
    • Meeting Reports
      • ACR Convergence
      • Other ACR meetings
      • EULAR/Other
    • Research Rheum
  • Drug Updates
    • Analgesics
    • Biologics/DMARDs
  • Practice Support
    • Billing/Coding
    • EMRs
    • Facility
    • Insurance
    • QA/QI
    • Technology
    • Workforce
  • Opinion
    • Patient Perspective
    • Profiles
    • Rheuminations
      • Video
    • Speak Out Rheum
  • Career
    • ACR ExamRheum
    • Awards
    • Career Development
  • ACR
    • ACR Home
    • ACR Convergence
    • ACR Guidelines
    • Journals
      • ACR Open Rheumatology
      • Arthritis & Rheumatology
      • Arthritis Care & Research
    • From the College
    • Events/CME
    • President’s Perspective
  • Search

Therapies Aimed at Immune Cell Progenitors May Be Key to Reducing Post Myocardial Infarction Risk

Lara C. Pullen, PhD  |  November 9, 2012

When fluorescent membrane dye-labeled HSPCs were adoptively transferred into a host, they settled in the bone marrow before the MI, and 52% migrated from the bone marrow post MI. The process appeared to be stem cell factor (SCF)–dependent because neutralization of SCF inhibited proliferation of host HSPCs as well as splenic retention of adoptively transferred HSPCs.

Although most scientists agree that atherosclerosis can be described as chronic inflammatory in nature, there is not yet an antiinflammatory therapy that is specific for atherosclerosis. “In my eyes, this opens up a new line of research and new therapeutic opportunities. In any inflammatory disease, including rheumatoid arthritis and atherosclerosis, we have to take the production of immune cells into account,” says Dr. Nahrendorf.

ad goes here:advert-1
ADVERTISEMENT
SCROLL TO CONTINUE

Dr. Pullen is a medical writer based in the Chicago area.

Reference

1. Dutta P, Courties G, Wei Y, et al. Myocardial infarction accelerates atherosclerosis. Nature. 2012;487:325-329.

ad goes here:advert-2
ADVERTISEMENT
SCROLL TO CONTINUE

 

Page: 1 2 | Single Page
Share: 

Filed under:ConditionsResearch Rheum Tagged with:atherosclerosisMyocardial infarction

Related Articles

    Apolipoprotein E Polymorphism Associated with Hyperuricemia in Chinese Population

    December 12, 2014

    Researchers find link between hyperuricemia and higher serum uric acid levels in patients with APOE ε2ε3 genotype and APOE-ε2 allele

    A Heart In Danger

    November 1, 2006

    Rheumatologists should monitor and aggressively treat cardiac risk factors in patients with lupus and rheumatoid arthritis

    A Duet of Bone and the Immune System

    July 12, 2011

    Examining emerging perspectives in osteoimmunology

    Cellular Therapy of Autoimmune Disease

    November 1, 2008

    Is a novel treatment breakthrough on the horizon?

  • About Us
  • Meet the Editors
  • Issue Archives
  • Contribute
  • Advertise
  • Contact Us
  • Copyright © 2025 by John Wiley & Sons, Inc. All rights reserved, including rights for text and data mining and training of artificial technologies or similar technologies. ISSN 1931-3268 (print). ISSN 1931-3209 (online).
  • DEI Statement
  • Privacy Policy
  • Terms of Use
  • Cookie Preferences