Hypertrophic Cardiomyopathy 30, Atrial: Disease-Characteristics Report

Executive summary and evidence boundary

Hypertrophic cardiomyopathy 30, atrial is an exceptionally rare, recently delineated Mendelian cardiomyopathy associated with CORIN, the gene encoding the cardiac transmembrane serine protease corin. Its defining clinical spectrum is better described as left-atrial cardiomyopathy with hypertension, atrial arrhythmia, and fibrosis than as conventional sarcomeric, left-ventricular hypertrophic cardiomyopathy. Open Targets maps the entity to MONDO:0958241, CORIN/ENSG00000145244, PMID 37913506, and ClinVar records RCV003882741 and RCV005234881. (OpenTargets Search: Hypertrophic cardiomyopathy 30, atrial)

The evidence base is extremely small. The pivotal human report is Feldman et al., New England Journal of Medicine, published 2 November 2023, PMID 37913506, DOI: 10.1056/NEJMoa2301908. Its full text and detailed pedigree tables were not retrievable through the available tools. Consequently, exact family size, nucleotide/protein variant, allele frequency, segregation, penetrance, and patient-level frequencies should be curated directly from that article and its ClinVar submissions rather than inferred. The strongest accessible mechanistic evidence comes from CORIN-null mice, pressure-overload models, fibroblast experiments, and human cardiomyopathy transcriptomic analyses. (OpenTargets Search: Hypertrophic cardiomyopathy 30, atrial, niu2023corindeficiencyimpairs pages 12-13, kan2024progressionfromcardiomyopathy pages 1-2)

The following table distinguishes disease-specific observations from broader CORIN biology and general-HCM extrapolation.

Table: This table condenses the currently recoverable knowledge-base-ready facts for Hypertrophic Cardiomyopathy 30, Atrial and clearly separates disease-specific evidence from inferences based on broader CORIN biology and general HCM practice.

1. Disease information

Definition

This is a familial cardiac disorder attributed to impaired CORIN function and characterized principally by structural and electrical disease of the atrium, including atrial remodeling/fibrosis, atrial arrhythmia, and associated hypertension. The nomenclature “hypertrophic cardiomyopathy 30, atrial” should not be assumed to mean that conventional unexplained left-ventricular hypertrophy is obligatory; the accessible disease-specific evidence instead emphasizes a left-atrial phenotype. (OpenTargets Search: Hypertrophic cardiomyopathy 30, atrial)

Identifiers and synonyms

• MONDO: MONDO:0958241.
• Preferred database label: cardiomyopathy, familial hypertrophic, 30, atrial.
• Synonyms: hypertrophic cardiomyopathy 30, atrial; HCM30, atrial; CORIN-related atrial cardiomyopathy; familial left-atrial cardiomyopathy associated with CORIN.
• Gene: CORIN; Ensembl ENSG00000145244; approved protein name “corin, serine peptidase.”
• ClinVar disease records surfaced: RCV003882741 and RCV005234881.
• OMIM, Orphanet, MeSH, ICD-10/ICD-11: a distinct code could not be verified from retrieved evidence. Until confirmed, use broader cardiomyopathy/atrial-cardiomyopathy codes and preserve MONDO:0958241 as the specific computational identifier. (OpenTargets Search: Hypertrophic cardiomyopathy 30, atrial)

The source is an aggregated disease-level entity built from a family report and variant databases, not an EHR-derived population phenotype.

2. Etiology

Causal factor

The nominated cause is a germline CORIN defect. Corin normally converts pro-atrial natriuretic peptide (pro-ANP) to active ANP. Reduced activity therefore weakens natriuretic-peptide signaling, favors sodium retention and hypertension, and removes anti-hypertrophic and anti-fibrotic restraint. (kan2024progressionfromcardiomyopathy pages 17-17, niu2023corindeficiencyimpairs pages 1-2)

Risk factors and modifiers

• Genetic: a disease-associated CORIN variant is the primary risk factor. Exact HGVS nomenclature, ACMG/AMP classification, zygosity, population frequency, and segregation require direct ClinVar/PMID 37913506 review.
• Family history: relevant because the disorder is familial, but penetrance and age dependence are not yet quantifiable.
• Environmental/physiologic: high sodium intake, uncontrolled blood pressure, and chronic pressure load are biologically plausible aggravators, not proven human modifiers of this exact subtype. In mice, Corin loss produces salt-sensitive hypertension, while transverse aortic constriction markedly accelerates dysfunction. (niu2023corindeficiencyimpairs pages 12-13, niu2023corindeficiencyimpairs pages 1-2)
• Age: aging unmasks disease in CORIN-null mice; hypertrophy and fibrosis become evident after approximately nine months, with dysfunction prominent by 12 months. Human age-specific risk is unknown. (niu2023corindeficiencyimpairs pages 12-13, niu2023corindeficiencyimpairs pages 1-2)

No validated protective allele, modifier gene, sex-specific risk, occupational exposure, toxin, infection, diet, or pharmacogenomic association has been established for the named disorder. Blood-pressure control and avoidance of excessive sodium are reasonable phenotype-directed precautions, not demonstrated primary prevention.

3. Phenotypes

Disease-specific quantitative frequencies are unavailable. Suggested phenotypes are therefore separated into reported/core, mechanistically supported, and possible complications.

• Left-atrial cardiomyopathy/remodeling: core structural manifestation; likely chronic and progressive. Suggested HPO labels: abnormality of the left atrium, left atrial enlargement, and cardiomyopathy.
• Atrial arrhythmia, particularly atrial fibrillation: core electrical manifestation; potentially episodic initially and persistent later. HPO: atrial arrhythmia, atrial fibrillation.
• Cardiac fibrosis: core tissue manifestation and probable arrhythmogenic substrate. HPO: myocardial fibrosis/cardiac fibrosis.
• Hypertension: prominent associated systemic sign. HPO: systemic arterial hypertension.
• Cardiac hypertrophy: supported by the disease name and CORIN-deficiency models, but the relative atrial versus ventricular distribution in human carriers must not be inferred without the primary report. HPO: cardiac hypertrophy or left ventricular hypertrophy only if documented in the individual.
• Heart failure, pulmonary edema, reduced ejection fraction: plausible advanced consequences supported by models and broader cardiomyopathy data, but not established as universal disease-specific findings. (OpenTargets Search: Hypertrophic cardiomyopathy 30, atrial, niu2023corindeficiencyimpairs pages 12-13, kan2024progressionfromcardiomyopathy pages 1-2)

Potential quality-of-life effects include palpitations, exertional intolerance, anxiety concerning arrhythmia/stroke, medication burden, and limitations from heart failure. No disease-specific EQ-5D, SF-36, PROMIS, or functional-outcome study is available.

4. Genetic and molecular information

Gene and protein

CORIN encodes a type-II transmembrane serine protease expressed predominantly on cardiomyocyte surfaces. It activates pro-ANP; related literature also implicates corin in pro-BNP processing, sodium homeostasis, vascular remodeling, and blood-pressure regulation. (kan2024progressionfromcardiomyopathy pages 17-17, niu2023corindeficiencyimpairs pages 13-13, niu2023corindeficiencyimpairs pages 1-2)

Variant evidence

Open Targets links CORIN to the disease through PMID 37913506 and two ClinVar records. However, the accessible evidence does not safely establish the exact variant, transcript, HGVS expression, ACMG class, molecular consequence, or gnomAD/TOPMed frequency. Those fields should be marked pending primary-source verification, not populated from secondary inference. The disorder should be treated as germline/familial; no somatic etiology is implicated. (OpenTargets Search: Hypertrophic cardiomyopathy 30, atrial)

No validated modifier genes, epigenetic signature, recurrent structural variant, chromosomal rearrangement, anticipation, germline mosaicism, founder effect, or consanguinity association is known.

5. Environmental and lifestyle information

No environmental agent or infection causes this Mendelian disease. Physiologic stressors could nevertheless alter expression:

1. Increased sodium/volume burden may amplify hypertension when ANP activation is impaired.
2. Chronic hypertension raises atrial and ventricular wall stress.
3. Pressure overload promotes hypertrophy, fibroblast activation, and fibrosis.
4. Fibrosis creates an arrhythmogenic substrate and may impair filling and pump function.

This gene–environment chain is strongly supported in CORIN-null mice but remains unquantified in affected humans. Corin-null mice have impaired sodium handling and a systolic pressure around 118 mmHg versus 107 mmHg in wild-type controls. (niu2023corindeficiencyimpairs pages 1-2)

Smoking, alcohol, obesity, sleep apnea, and extreme exercise should be assessed because they affect atrial fibrillation and cardiomyopathy generally, but they have not been demonstrated as CORIN-specific modifiers.

6. Mechanism and pathophysiology

Proposed causal chain

Upstream: deleterious CORIN variation → reduced cell-surface corin abundance, activation, or protease function → deficient pro-ANP cleavage.

Intermediate: reduced mature ANP → reduced natriuretic-peptide receptor-A/cGMP/PKG signaling → diminished natriuresis and vasodilation plus inadequate suppression of renin–angiotensin–aldosterone signaling.

Downstream: sodium/volume retention and hypertension → atrial wall stress and pressure loading → cardiomyocyte hypertrophy and cardiac-fibroblast activation → extracellular-matrix deposition/fibrosis → atrial electrical remodeling and arrhythmia; prolonged disease may progress to ventricular dysfunction, heart failure, and pulmonary edema. (kan2024progressionfromcardiomyopathy pages 17-17, niu2023corindeficiencyimpairs pages 12-13, niu2023corindeficiencyimpairs pages 1-2)

A direct experimental quote from the 2023 mouse study summarizes the rescue evidence: “Corin deficiency impairs cardiac function and exacerbates HF development in mice.” Recombinant soluble corin increased plasma cGMP, reduced N-terminal pro-ANP, angiotensin II, and aldosterone, and ameliorated hypertrophy, fibrosis, dysfunction, and lung edema after pressure overload. (niu2023corindeficiencyimpairs pages 12-13, niu2023corindeficiencyimpairs pages 1-2)

Molecular profiling

A 2024 analysis integrated bulk transcriptomic data from 106 HCM and 184 dilated-cardiomyopathy patients with single-nucleus RNA sequencing and Mendelian-randomization analyses. A low-CORIN/high-fibroblast-activation cluster was associated with lower ejection fraction and poorer prognosis. In neonatal-rat cardiac fibroblasts, CORIN overexpression reduced TGF-β1-induced COL1A1 and α-SMA expression. These results support an anti-fibrotic role but are not specific to MONDO:0958241; clinical covariates and independent subtype validation were limited. (kan2024progressionfromcardiomyopathy pages 1-2)

Suggested annotations:

• GO biological processes: proteolytic activation of peptide hormone; natriuretic peptide signaling; cGMP-mediated signaling; regulation of systemic arterial blood pressure; sodium-ion homeostasis; negative regulation of cardiac-muscle hypertrophy; extracellular-matrix organization; cardiac fibrosis.
• Cell Ontology: cardiomyocyte; atrial cardiomyocyte; cardiac fibroblast; vascular endothelial cell.
• GO cellular components: plasma membrane; cell surface; extracellular region.
• Chemical entities: ANP, cGMP, sodium ion, angiotensin II, aldosterone; CHEBI identifiers should be validated during ontology ingestion.

No disease-specific methylome, proteome, metabolome, lipidome, spatial-transcriptomic, CRISPR-screen, or patient-derived single-cell atlas was identified.

7. Anatomical structures affected

• Primary organ: heart.
• Principal site: left atrium/atrial myocardium; suggested UBERON labels: heart, left atrium, myocardium.
• Cells: atrial cardiomyocytes and cardiac fibroblasts.
• Subcellular site: cardiomyocyte plasma membrane/cell surface, where corin processes extracellular pro-ANP.
• Secondary systems: systemic vasculature and kidney through blood-pressure, volume, and sodium regulation; lungs may be involved secondarily through heart-failure pulmonary edema.
• Lateralization: not applicable beyond specific left-atrial predominance; unilateral/bilateral terminology is inappropriate. (kan2024progressionfromcardiomyopathy pages 17-17, niu2023corindeficiencyimpairs pages 12-13, niu2023corindeficiencyimpairs pages 1-2)

8. Temporal development

Human onset, median diagnostic age, and progression rate are unknown. The familial phenotype is most reasonably regarded as chronic, potentially age-dependent, and variably expressive pending longitudinal study.

The model-organism trajectory is clearer: CORIN-null mice develop hypertension first, then hypertrophy and fibrosis after about nine months, and progressive dysfunction by roughly 12 months. Pressure overload at 10–12 weeks precipitates more rapid deterioration than in wild-type mice. This suggests a latent compensated phase followed by stress- or age-associated decompensation, but mouse timing cannot be directly translated to patients. (niu2023corindeficiencyimpairs pages 12-13, niu2023corindeficiencyimpairs pages 1-2)

No spontaneous remission, treatment-induced molecular remission, or critical pediatric intervention window has been demonstrated.

9. Inheritance and population

The disease is familial and Mendelian, but the precise inheritance mode and penetrance could not be verified from accessible primary text. An autosomal-dominant model may be plausible for a multigenerational familial cardiomyopathy, but it should remain unconfirmed until the pedigree and ClinVar records are reviewed.

There are no reliable estimates of prevalence, incidence, carrier frequency, sex ratio, ethnic enrichment, geographic distribution, founder effect, or age distribution. It should be classified as ultra-rare rather than assigned a numerical prevalence. General HCM prevalence must not be substituted for CORIN-related atrial cardiomyopathy.

10. Diagnostics

Clinical evaluation

A rational work-up is:

1. Three-generation pedigree, blood-pressure history, symptoms, and medication/exposure review.
2. Resting 12-lead ECG and ambulatory rhythm monitoring to detect atrial fibrillation or other atrial arrhythmias.
3. Transthoracic echocardiography, emphasizing atrial size/function, ventricular wall thickness, diastolic function, ejection fraction, and outflow obstruction.
4. Cardiac MRI for atrial/ventricular morphology and late-gadolinium-enhancement fibrosis where technically appropriate.
5. Biomarkers such as NT-proBNP/BNP, renal function, electrolytes, and troponin when clinically indicated. Pro-ANP processing or soluble corin is mechanistically attractive but not a validated disease-specific diagnostic assay.
6. Exclude secondary hypertrophy/remodeling: long-standing hypertension, valve disease, athlete’s heart, infiltrative/storage disorders, sarcomeric HCM, congenital structural disease, and tachycardia-mediated remodeling.

Genetic testing

Use a validated cardiomyopathy/arrhythmia panel that includes CORIN, with deletion/duplication analysis as appropriate. If negative despite a compelling family phenotype, consider exome or genome sequencing and periodic reanalysis. A confirmed familial pathogenic/likely pathogenic variant enables cascade testing; relatives without definitive molecular clarification require longitudinal ECG and imaging surveillance.

General-HCM data indicate that targeted testing yields a causal variant in about 30% of sporadic cases and up to 60% of familial or younger, typical cases, but these figures cannot be applied to this CORIN entity. A 2024 review recommends disease-focused next-generation-sequencing panels and cascade testing when a decisively pathogenic familial variant is found. Abbas et al., 20 March 2024, DOI 10.3390/biomedicines12030682. No evidence supports routine karyotyping, FISH, mitochondrial sequencing, repeat-expansion testing, liquid biopsy, or diagnostic proteomics for this disorder.

11. Outcome and prognosis

No disease-specific survival curve, mortality rate, life-expectancy estimate, stroke rate, heart-failure rate, or quality-of-life dataset exists in accessible evidence. Plausible complications include persistent atrial fibrillation, thromboembolism/stroke, progressive fibrosis, hypertension-mediated organ damage, heart failure, and—if ventricular disease is present—ventricular arrhythmia or sudden cardiac death. These require individual risk assessment rather than assumed attribution.

In broader cardiomyopathy datasets, reduced CORIN expression is associated with lower ejection fraction and worse prognosis, while CORIN-null mice develop progressive dysfunction and fibrosis. These observations establish biological concern but not patient-level prognostic calibration for HCM30. (kan2024progressionfromcardiomyopathy pages 17-17, kan2024progressionfromcardiomyopathy pages 1-2)

Potential prognostic measurements include atrial size and strain, atrial-fibrillation burden, fibrosis on MRI, blood-pressure control, ventricular thickness/function, NT-proBNP, and clinical heart-failure status. None is yet validated specifically for CORIN-related disease.

12. Treatment

There is no approved CORIN-genotype-specific therapy and no disease-specific clinical trial identified. Current care should be phenotype-directed at a cardiomyopathy center.

• Hypertension/volume control: individualized antihypertensive therapy and avoidance of excessive sodium; avoid abrupt preload reduction if significant obstructive ventricular physiology exists.
• Atrial fibrillation: rhythm/rate control as appropriate and thromboembolic-risk management. In established HCM with clinical AF, contemporary guidelines generally favor anticoagulation irrespective of conventional CHA₂DS₂-VASc thresholds, but whether every isolated CORIN atrial phenotype meets that HCM rule requires specialist judgment.
• Heart failure: guideline-directed therapy matched to ejection fraction and hemodynamics.
• Obstructive ventricular HCM, if independently documented: non-vasodilating beta-blocker first; verapamil/diltiazem when appropriate; disopyramide, septal reduction, or a cardiac-myosin inhibitor in eligible patients. These interventions target ventricular sarcomeric hypercontractility and are not validated for isolated CORIN-mediated atrial disease.
• Devices/ablation: catheter ablation, pacemaker, or ICD only for standard rhythm and sudden-death indications, not genotype alone.
• Support: genetic counseling, family screening, exercise counseling, pregnancy planning, and management of obesity/sleep apnea and other AF-promoting conditions.

The authoritative current frameworks are the 2023 ESC cardiomyopathy guideline and 2024 AHA/ACC/AMSSM/HRS/PACES/SCMR HCM guideline (published June 2024; DOI 10.1161/CIR.0000000000001250). A systematic comparison found broad agreement on echocardiography, genetic testing/family screening, medical and invasive management, exercise, and reproductive counseling, with differences in diagnostic definitions, MRI use, and sudden-death risk assessment.

Recombinant soluble corin is an experimental concept only. In pressure-overloaded knockout mice it increased cGMP and reduced RAAS activation, hypertrophy, fibrosis, and edema; no human efficacy, dose, safety, immunogenicity, or delivery data support clinical use. (niu2023corindeficiencyimpairs pages 12-13, niu2023corindeficiencyimpairs pages 1-2)

Suggested NCIT intervention labels: genetic counseling; electrocardiography; ambulatory ECG monitoring; echocardiography; cardiac MRI; antihypertensive therapy; anticoagulation therapy; antiarrhythmic therapy; catheter ablation; implantable cardioverter-defibrillator; septal myectomy. Validate exact NCIT codes during ingestion.

13. Prevention

• Primary prevention: the inherited variant cannot currently be prevented. Reproductive options after molecular confirmation include prenatal diagnosis and preimplantation genetic testing with nondirective counseling.
• Secondary prevention: cascade genetic testing, ECG/rhythm surveillance, echocardiography, MRI when indicated, and early detection/control of hypertension and atrial arrhythmia.
• Tertiary prevention: blood-pressure control, stroke prevention in AF, heart-failure therapy, and individualized arrhythmic-risk management.
• Behavioral measures: avoid smoking and stimulant misuse; maintain healthy weight; diagnose sleep apnea; use individualized exercise advice; avoid excessive sodium and alcohol where hypertension/AF is present.
• Vaccination/public-health control: no disease-specific vaccine or infectious prophylaxis applies.

No intervention has been shown to prevent phenoconversion in genotype-positive CORIN carriers.

14. Other species and natural disease

No verified naturally occurring CORIN-associated counterpart in companion animals, livestock, or wildlife was identified. There is no zoonotic transmission. CORIN is evolutionarily conserved, and experimental mouse phenotypes demonstrate conservation of natriuretic-peptide activation and blood-pressure regulation, but engineered knockout disease should not be entered as naturally occurring veterinary HCM30.

Suggested taxonomy for the principal experimental species: Mus musculus (NCBI Taxon 10090). Exact mouse Corin and ortholog gene identifiers should be imported from NCBI Gene/Alliance rather than inferred here.

15. Model organisms and experimental systems

Mouse models

• Constitutive Corin knockout: salt-sensitive hypertension, progressive cardiac hypertrophy and fibrosis after nine months, and later dysfunction. Strength: models systemic loss of corin. Limitation: the human variant may be hypomorphic or domain-specific, and the mouse phenotype is not selectively atrial. (niu2023corindeficiencyimpairs pages 12-13, niu2023corindeficiencyimpairs pages 1-2)
• Corin knockout plus transverse aortic constriction: at 10–12 weeks, knockout mice deteriorate faster than similarly stressed wild types, modeling gene–pressure-load interaction. Recombinant soluble corin partially rescues function, morphology, cGMP signaling, RAAS activation, and pulmonary edema. Strength: causal perturbation and rescue. Limitation: surgically imposed ventricular afterload differs from spontaneous human atrial disease. (niu2023corindeficiencyimpairs pages 12-13, niu2023corindeficiencyimpairs pages 1-2)
• Conditional cardiac/renal Corin models: useful for separating endocrine cardiac CORIN from renal or intestinal sodium-handling effects; these are mechanistic models rather than faithful replicas of HCM30.

Cellular and computational systems

Neonatal-rat cardiac fibroblasts exposed to TGF-β1 show reduced COL1A1 and α-SMA activation after CORIN overexpression. Human HCM/DCM bulk and single-nucleus transcriptomic analyses identify low-CORIN, fibroblast-rich disease clusters. These systems support anti-fibrotic activity but cannot establish variant-specific atrial causality. (kan2024progressionfromcardiomyopathy pages 1-2)

High-priority future models are patient-derived iPSC atrial cardiomyocytes and fibroblasts, isogenic CRISPR correction/knock-in lines, atrial engineered tissues, and variant-specific knock-in mice. Required readouts include pro-ANP cleavage, cell-surface CORIN abundance, cGMP/PKG activity, electrophysiology, conduction, extracellular-matrix production, and response to pressure/sodium stress.

Key evidence gaps and curation priorities

1. Retrieve PMID 37913506 and ClinVar RCV003882741/RCV005234881 to capture exact HGVS variant, transcript, zygosity, ACMG class, family size, segregation, and functional assays.
2. Determine whether inheritance is definitively autosomal dominant and quantify age-dependent penetrance.
3. Separate atrial hypertrophy/remodeling from ventricular HCM in the formal disease definition.
4. Obtain individual-level phenotype frequencies, onset, rhythm burden, fibrosis measurements, blood-pressure data, treatment responses, and outcomes.
5. Establish whether soluble corin, pro-ANP:mature-ANP ratio, or cGMP is diagnostically or prognostically useful.
6. Develop variant-specific human atrial models and a prospective international registry.

Overall, the association of CORIN with MONDO:0958241 is supported, and the CORIN–ANP–cGMP/RAAS axis provides a coherent causal mechanism. Nevertheless, most clinical implementation currently rests on phenotype-directed cardiomyopathy and atrial-arrhythmia practice, while exact molecular and natural-history annotations remain dependent on direct curation of the foundational 2023 family report. (OpenTargets Search: Hypertrophic cardiomyopathy 30, atrial, niu2023corindeficiencyimpairs pages 12-13, kan2024progressionfromcardiomyopathy pages 1-2, niu2023corindeficiencyimpairs pages 1-2)

References

1. (OpenTargets Search: Hypertrophic cardiomyopathy 30, atrial): Open Targets Query (Hypertrophic cardiomyopathy 30, atrial, 1 results). Buniello, A. et al. (2025). Open Targets Platform: facilitating therapeutic hypotheses building in drug discovery. Nucleic Acids Research.

2. (niu2023corindeficiencyimpairs pages 12-13): Yayan Niu, Tiantian Zhou, Shengnan Zhang, Wenguo Li, Kun Wang, Ningzheng Dong, and Qingyu Wu. Corin deficiency impairs cardiac function in mouse models of heart failure. Frontiers in Cardiovascular Medicine, Aug 2023. URL: https://doi.org/10.3389/fcvm.2023.1164524, doi:10.3389/fcvm.2023.1164524. This article has 11 citations and is from a peer-reviewed journal.

3. (kan2024progressionfromcardiomyopathy pages 1-2): Jun-yan Kan, Dong-chen Wang, Zi-hao Jiang, Li-da Wu, Ke Xu, and Yue Gu. Progression from cardiomyopathy to heart failure with reduced ejection fraction: a corin deficient course. Heliyon, 10:e37838, Sep 2024. URL: https://doi.org/10.1016/j.heliyon.2024.e37838, doi:10.1016/j.heliyon.2024.e37838. This article has 2 citations.

4. (niu2023corindeficiencyimpairs pages 1-2): Yayan Niu, Tiantian Zhou, Shengnan Zhang, Wenguo Li, Kun Wang, Ningzheng Dong, and Qingyu Wu. Corin deficiency impairs cardiac function in mouse models of heart failure. Frontiers in Cardiovascular Medicine, Aug 2023. URL: https://doi.org/10.3389/fcvm.2023.1164524, doi:10.3389/fcvm.2023.1164524. This article has 11 citations and is from a peer-reviewed journal.

5. (kan2024progressionfromcardiomyopathy pages 17-17): Jun-yan Kan, Dong-chen Wang, Zi-hao Jiang, Li-da Wu, Ke Xu, and Yue Gu. Progression from cardiomyopathy to heart failure with reduced ejection fraction: a corin deficient course. Heliyon, 10:e37838, Sep 2024. URL: https://doi.org/10.1016/j.heliyon.2024.e37838, doi:10.1016/j.heliyon.2024.e37838. This article has 2 citations.

6. (niu2023corindeficiencyimpairs pages 13-13): Yayan Niu, Tiantian Zhou, Shengnan Zhang, Wenguo Li, Kun Wang, Ningzheng Dong, and Qingyu Wu. Corin deficiency impairs cardiac function in mouse models of heart failure. Frontiers in Cardiovascular Medicine, Aug 2023. URL: https://doi.org/10.3389/fcvm.2023.1164524, doi:10.3389/fcvm.2023.1164524. This article has 11 citations and is from a peer-reviewed journal.

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