Author + information
- Received May 21, 2019
- Revision received January 29, 2020
- Accepted January 29, 2020
- Published online May 25, 2020.
- Shuin Park, BSa,b,c,
- Sara Ranjbarvaziri, PhDa,b,c,∗,
- Peng Zhao, MD, PhDa and
- Reza Ardehali, MD, PhDa,b,c,d,∗ ()
- aDivision of Cardiology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles (UCLA), Los Angeles, California
- bEli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, University of California, Los Angeles (UCLA), Los Angeles, California
- cMolecular, Cellular, and Integrative Physiology Graduate Program, University of California, Los Angeles (UCLA), Los Angeles, California
- dMolecular Biology Institute, UCLA, Los Angeles, California
- ↵∗Address for correspondence:
Dr. Reza Ardehali, University of California, Los Angeles, Division of Cardiology, Department of Medicine, University of California-Los Angeles, 675 Charles E. Young Drive South, Room 3645, Los Angeles, California 90095-1760.
• After in vitro stimulation or in vivo pressure overload injury, activated cardiac fibroblasts express Ltbp2, Comp, and Cilp.
• In ischemic heart disease, LTBP2, COMP, and CILP localize to the fibrotic regions of the injured heart.
• Circulating levels of full-length CILP are decreased in patients with heart failure, suggestive of the potential to use this protein as a biomarker for the presence of cardiac fibrosis.
Cardiac fibrosis is a pathological process associated with various forms of heart failure. This study identified latent transforming growth factor-β binding protein 2, cartilage oligomeric matrix protein, and cartilage intermediate layer protein 1 as potential biomarkers for cardiac fibrosis. All 3 encoded proteins showed increased expression in fibroblasts after transforming growth factor-β stimulation in vitro and localized specifically to fibrotic regions in vivo. Of the 3, only the full-length cartilage intermediate layer protein 1 showed a significant decrease in circulating levels in patients with heart failure compared with healthy volunteers. Further studies on these 3 proteins will lead to a better understanding of their biomarker potential for cardiac fibrosis.
↵∗ Current address: Department of Pediatrics and Cardiovascular Institute, Stanford University, Stanford, California.
This work was supported in part by the National Institute of Health DP2 (HL127728) and AHA Innovative Project Award (18IPA34170309). Ms. Park was supported by the Ruth L. Kirschstein National Research Service Award (T32HL69766). All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACC: Basic to Translational Science author instructions page.
- Received May 21, 2019.
- Revision received January 29, 2020.
- Accepted January 29, 2020.
- 2020 The Authors