ArticleThe Journal of clinical investigation2015
Cardiomyocyte-enriched protein CIP protects against pathophysiological stresses and regulates cardiac homeostasis.
Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Genome-wide association and multi-trait analyses characterize the common genetic architecture of heart failure.Nature communications · 2022Pooled it
- MLIP genotype as a predictor of pharmacological response in primary open-angle glaucoma and ocular hypertension.Scientific reports · 2021Trial
- Treatment with the Nox1/4 inhibitor Setanaxib ameliorates cardiac function in mouse models of Duchenne muscular dystrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Small Extracellular Vesicle External Surface Adiponectin-Mediated Adipocytes/Cardiomyocytes Communication in Diabetic Ischemic Heart Failure.Circulation · 2026Article
- Persistence of dysfunctional immune response 12 months after SARS-CoV-2 infection and their relationship with pulmonary sequelae and long COVID.Respiratory research · 2025Article
- Large-scale multi-omics identifies drug targets for heart failure with reduced and preserved ejection fraction.Nature cardiovascular research · 2025Article
- Therapeutic Inhibition ofCirculation research · 2024Article
- Review
- Article
- A novel interleukin-2-based fusion molecule, HCW9302, differentially promotes regulatory T cell expansion to treat atherosclerosis in mice.Frontiers in immunology · 2023Article
- The effects of β-catenin on cardiomyogenesis via Islet-1 and MLIP ubiquitination.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- Targeting Adiponectin Receptor 1 Phosphorylation Against Ischemic Heart Failure.Circulation research · 2022Article
- Novel homozygous nonsense mutation of MLIP and compensatory alternative splicing.NPJ genomic medicine · 2022Article
- Cardiac CIP protein regulates dystrophic cardiomyopathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Neuromuscular disease: 2022 update.Free neuropathology · 2022Article
- Cardiac ISL1-Interacting Protein, a Cardioprotective Factor, Inhibits the Transition From Cardiac Hypertrophy to Heart Failure.Frontiers in cardiovascular medicine · 2022Article
- Loss of mFrontiers in cardiovascular medicine · 2022Article
- MLIP causes recessive myopathy with rhabdomyolysis, myalgia and baseline elevated serum creatine kinase.Brain : a journal of neurology · 2021Article
- LncRNA LncHrt preserves cardiac metabolic homeostasis and heart function by modulating the LKB1-AMPK signaling pathway.Basic research in cardiology · 2021Article
- Muscle Enriched Lamin Interacting Protein (Cells · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 4 institutions in 4 countries.
Funding
Abstract
Cardiomyopathy is a common human disorder that is characterized by contractile dysfunction and cardiac remodeling. Genetic mutations and altered expression of genes encoding many signaling molecules and contractile proteins are associated with cardiomyopathy; however, how cardiomyocytes sense pathophysiological stresses in order to then modulate cardiac remodeling remains poorly understood. Here, we have described a regulator in the heart that harmonizes the progression of cardiac hypertrophy and dilation. We determined that expression of the myocyte-enriched protein cardiac ISL1-interacting protein (CIP, also known as MLIP) is reduced in patients with dilated cardiomyopathy. As CIP is highly conserved between human and mouse, we evaluated the effects of CIP deficiency on cardiac remodeling in mice. Deletion of the CIP-encoding gene accelerated progress from hypertrophy to heart failure in several cardiomyopathy models. Conversely, transgenic and AAV-mediated CIP overexpression prevented pathologic remodeling and preserved cardiac function. CIP deficiency combined with lamin A/C deletion resulted in severe dilated cardiomyopathy and cardiac dysfunction in the absence of stress. Transcriptome analyses of CIP-deficient hearts revealed that the p53- and FOXO1-mediated gene networks related to homeostasis are disturbed upon pressure overload stress. Moreover, FOXO1 overexpression suppressed stress-induced cardiomyocyte hypertrophy in CIP-deficient cardiomyocytes. Our studies identify CIP as a key regulator of cardiomyopathy that has potential as a therapeutic target to attenuate heart failure progression.
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What OpenQuestion holds
Registered trials
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.