ArticleJCI insight2022
FAM114A1 influences cardiac pathological remodeling by regulating angiotensin II signaling.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
- Altered Functional Specialization and Interhemispheric Coordination in Rhegmatogenous Retinal Detachment: Associations With Gene Expression, Neurotransmitter Receptor Distribution, and SVM-SHAP ClassificationCNS neuroscience & therapeutics · 2026Article
- Family with sequence similarity 114 member A1 orchestrates immune evasion in triple-negative breast cancer.Signal transduction and targeted therapy · 2025Article
- Genetic variants affecting RNA stability influence complex traits and disease risk.Nature genetics · 2025Article
- Annexin-A1 deficiency uncovers female-specific pathways in blood pressure control and cardiovascular remodeling in mice.Communications biology · 2025Article
- Genomic structural equation modeling elucidates the shared genetic architecture of allergic disorders.Journal of translational medicine · 2025Article
- Microrna363-5p targets thrombospondin3 to regulate pathological cardiac remodeling.Molecular and cellular biochemistry · 2025Article
- Article
- Deficiency of the sphingosine-1-phosphate (S1P) transporter Mfsd2b protects the heart against hypertension-induced cardiac remodeling by suppressing the L-type-CaBasic research in cardiology · 2024Article
- Fibroblasts and immune cells: at the crossroad of organ inflammation and fibrosis.American journal of physiology. Heart and circulatory physiology · 2024Review
- Cardiomyocyte intercellular signalling increases oxidative stress and reprograms the global- and phospho-proteome of cardiac fibroblasts.Journal of extracellular biology · 2023Article
- miR-125a-5p/miR-125b-5p contributes to pathological activation of angiotensin II-AT1R in mouse distal convoluted tubule cells by the suppression of Atrap.The Journal of biological chemistry · 2023Article
- Fucoxanthin inhibits cardiac fibroblast transdifferentiation by alleviating oxidative stress through downregulation of BRD4.PloS one · 2023Article
- Treatment of myocardial interstitial fibrosis in pathological myocardial hypertrophy.Frontiers in pharmacology · 2022Review
- A Boolean approach for novel hypoxia-related gene discovery.PloS one · 2022Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Cardiac pathological remodeling, a primary contributor to heart failure (HF) and death, is an important target for HF therapy. However, the signaling pathways that govern cardiac remodeling are not fully elucidated. Here, we found that a functionally unannotated human myocardial infarction-associated (MI-associated) gene, family with sequence similarity 114 member A1 (FAM114A1), is induced in failing human and mouse hearts compared with nonfailing hearts. Homozygous KO of Fam114a1 (Fam114a1-/-) in the mouse genome reduces cardiomyocyte hypertrophy, inflammation, and cardiac fibrosis while restoring cardiac function in angiotensin II-induced (Ang II-induced) and MI-induced HF mouse models. Cardiac fibroblasts (CFs) exhibit the highest FAM114A1 expression among different cardiac cell types. FAM114A1 is a critical autonomous factor for CF proliferation, activation, and migration. Mechanistically, FAM114A1 interacts with angiotensin receptor-associated protein (AGTRAP) and regulates the expression of angiotensin type 1 receptor (AT1R) and downstream Ang II signaling transduction, and it subsequently influences profibrotic response. Our results indicate that FAM114A1 regulates Ang II signaling, thereby activating CFs and other cardiac cells and augmenting pathological cardiac remodeling. These findings provide potentially novel insights into the regulation of cardiac remodeling and identify FAM114A1 as a therapeutic target for the treatment of heart disease.
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