FICD (FIC Domain Protein Adenylyl Transferase) Deficiency Protects Mice From Hypertrophy‐Induced Heart Failure and Promotes BiP (Binding Immunoglobulin Protein) ‐Mediated Activation of the Unfolded Protein Response and Endoplasmic Reticulum‐Selective
Our results highlight a novel regulatory paradigm controlling stress resilience in cardiomyocytes and offer a rationale to consider FICD as a therapeutic target to treat cardiac hypertrophy.
Authors
- Shannon M. Lacy (ORCID: https://orcid.org/0000-0001-8730-0791)
- Daniel E. Michele (ORCID: https://orcid.org/0000-0003-4393-4551)
- Eric D. Smith (ORCID: https://orcid.org/0000-0002-5915-9492)
- Adam S. Helms (ORCID: https://orcid.org/0000-0002-0234-6430)
- Nicholas D. Urban (ORCID: https://orcid.org/0000-0002-4677-789X)
- Matthias C. Truttmann (ORCID: https://orcid.org/0000-0002-0536-7923)
- Rebecca J. Taubitz
- Samantha N. Turowski (ORCID: https://orcid.org/0009-0002-7452-6964)
- Eric N. Primack
Institutions
- University of Michigan (US)
- Michigan Medicine (US)
Publication Details
- Journal
- Journal of the American Heart Association
- Published
- 2025-08-18
- DOI
- https://doi.org/10.1161/jaha.124.040192
- Citations
- 5
- Primary Topic
- Endoplasmic Reticulum Stress and Disease
- Type
- article
- Field-Weighted Citation Impact
- 5.76