Cardiomyopathy, Dilated, 100 (DCM100): Research Report

Executive summary and evidence limits

Cardiomyopathy, dilated, 100 (DCM100) is an exceptionally rare Mendelian form of familial dilated cardiomyopathy associated with VEZF1 (vascular endothelial zinc finger 1). The exact disease is indexed as MONDO:0859381; OpenTargets links it to VEZF1 through the 2023 defining report, PMID 36657711. It must not be confused with the distinct, autosomal-recessive RPL3L-associated neonatal DCM. (OpenTargets Search: Cardiomyopathy Dilated 100)

The disease-specific evidence base is currently very small. One family report establishes the association, while most mechanistic information comes from human myocardial-expression datasets, zebrafish knockdown, and cultured rodent cardiomyocytes. Accordingly, claims below are labeled DCM100-specific, supportive experimental evidence, or generic-DCM extrapolation. Exact pedigree details, the reported HGVS variant, patient-level phenotype, OMIM number, penetrance, and variant frequency could not be verified from the accessible full text and are therefore not invented.

The following table provides the most compact knowledge-base representation.

Table: This table summarizes the highest-confidence facts currently recoverable for Cardiomyopathy, Dilated, 100, clearly separating disease-specific findings from broader DCM extrapolations. It is designed for direct knowledge-base ingestion with ontology suggestions and context-ID citations.

1. Disease information

Definition

DCM is a myocardial disorder characterized by ventricular—usually left-ventricular—dilatation and systolic dysfunction not adequately explained by abnormal loading conditions or coronary disease. Historical research criteria include fractional shortening <25% or left-ventricular ejection fraction <45%, together with LV end-diastolic diameter >117% of the value predicted for age and body-surface area. DCM100 denotes the VEZF1-associated familial subtype, rather than all DCM. (mcnally2017dilatedcardiomyopathygenetic pages 2-3)

Identifiers and synonyms

• Preferred name: Cardiomyopathy, dilated, 100
• Synonyms: Dilated cardiomyopathy 100; DCM100; VEZF1-related dilated cardiomyopathy
• MONDO: MONDO:0859381
• Causal gene: VEZF1, Ensembl ENSG00000136451
• Defining publication: Shi HY et al., VEZF1 loss-of-function mutation underlying familial dilated cardiomyopathy, European Journal of Medical Genetics, 2023; DOI: https://doi.org/10.1016/j.ejmg.2023.104705; PMID: https://pubmed.ncbi.nlm.nih.gov/36657711/ (OpenTargets Search: Cardiomyopathy Dilated 100)
• OMIM/Orphanet: an exact disease-level number was not independently recoverable from the available evidence.
• ICD-10: DCM generally maps to I42.0, but this is not specific to DCM100.
• ICD-11/MeSH: use the broader dilated-cardiomyopathy concepts; no subtype-specific code was verified.

The evidence is an aggregated disease-level synthesis based on a published family, experimental studies, and databases—not individual EHR data.

2. Etiology and risk factors

Causal factor

The defining human report attributes familial DCM to a VEZF1 loss-of-function mutation. The familial title and disease classification support autosomal-dominant transmission, but exact segregation counts and the variant’s HGVS description require confirmation from the original article before clinical use. OpenTargets records one disease–target evidence item tied to PMID 36657711. (OpenTargets Search: Cardiomyopathy Dilated 100)

Genetic and environmental risk

The principal established DCM100 risk is carriage of the familial VEZF1 variant. No independently replicated susceptibility loci, modifier genes, founder allele, carrier frequency, germline mosaicism, anticipation, or population-specific enrichment have been reported for this subtype in the retrieved evidence.

No DCM100-specific environmental risk or protective factor has been established. For DCM generally, myocardial stressors—viral myocarditis, alcohol, cardiotoxic drugs, pregnancy, endocrine/metabolic disease, sustained tachyarrhythmia, and hemodynamic overload—may precipitate or worsen ventricular dysfunction. Applying these as VEZF1 gene–environment interactions is biologically plausible but unproven.

Experimental data provide one candidate interaction: Vezf1-deficient zebrafish had a disproportionately impaired response to β-adrenergic stress, suggesting that reduced VEZF1 limits cardiac contractile reserve under increased demand. This is a model-organism observation, not demonstrated penetrance modification in human carriers. (paavola2020vezf1regulatescardiac pages 2-3, paavola2020vezf1regulatescardiac pages 8-9)

3. Phenotypes

The confidently assignable phenotype is dilated cardiomyopathy with ventricular systolic dysfunction. The accessible evidence does not support reliable DCM100-specific frequencies, onset ages, sex differences, or extracardiac manifestations.

Suggested terms include:

• Dilated cardiomyopathy — HP:0001644: defining structural/functional phenotype.
• Reduced left-ventricular ejection fraction — HP:0012664 or the current HPO equivalent used by the target database.
• Left-ventricular dilatation — HP:0001711.
• Congestive heart failure — HP:0001635: possible advanced manifestation.
• Cardiomegaly — HP:0001640, dyspnea — HP:0002094, exercise intolerance — HP:0003546, fatigue — HP:0012378, peripheral edema — HP:0012398, and cardiac arrhythmia — HP:0011675: clinically plausible generic DCM manifestations, but not confirmed as frequencies in DCM100.

DCM can impair exercise capacity, schooling or employment, sleep, independence, and psychosocial well-being. No DCM100-specific EQ-5D, SF-36, KCCQ, or pediatric quality-of-life data exist in the retrieved literature.

4. Genetic and molecular information

Gene and protein

VEZF1 encodes a highly conserved nuclear C2H2 zinc-finger transcription factor with six zinc-finger motifs and a proline-rich transactivation domain. It is expressed in endothelial cells and adult cardiomyocytes and participates in angiogenesis, cardiac growth, and transcriptional control of contractile genes. (paavola2020vezf1regulatescardiac pages 1-2, paavola2020vezf1regulatescardiac pages 11-12)

Variant evidence

The defining publication reports a loss-of-function mutation segregating with familial DCM. However, the following could not be independently recovered and should remain null fields pending inspection of the original article:

• HGVS genomic/cDNA/protein nomenclature;
• missense, nonsense, frameshift, or splice class;
• ClinVar classification and accession;
• gnomAD/TOPMed frequency;
• ACMG/AMP criteria;
• number of carriers and affected relatives;
• functional effect of the specific human allele.

The presumed origin is germline, given familial Mendelian transmission. There is no evidence that DCM100 is somatic. No validated modifier gene, pathogenic copy-number change, methylation signature, or disease-specific chromosomal abnormality is established.

5. Environmental information

No toxin, infection, radiation, occupational exposure, diet, smoking behavior, alcohol exposure, or pathogen has been shown to cause DCM100. These should be captured only as general DCM differential etiologies or possible secondary stressors—not as causes of the VEZF1 subtype.

Reasonable risk-reduction practice is avoidance of cardiotoxic exposures, recreational stimulants, heavy alcohol consumption, and unsupervised extreme exercise after cardiomyopathy is recognized. This is generic cardiomyopathy care rather than evidence for primary prevention of VEZF1 disease.

6. Mechanism and pathophysiology

Proposed causal chain

1. Upstream genetic event: reduced VEZF1 function.
2. Transcriptional dysregulation: altered VEZF1–TEAD1 regulation of muscle genes, including MYH7/β-myosin heavy chain, ATP1A2, TCAP, ACTA1, MYH11, and troponin genes.
3. Contractile-unit imbalance: reduced MYH7/β-MHC with increased skeletal α-actin lowers the myosin/actin ratio.
4. Cellular phenotype: reduced cardiomyocyte growth and shortening with impaired compensatory response to adrenergic/hemodynamic stress.
5. Organ phenotype: reduced contractile reserve, ventricular systolic dysfunction, remodeling, and DCM/heart failure. (paavola2020vezf1regulatescardiac pages 5-7, paavola2020vezf1regulatescardiac pages 7-8, paavola2020vezf1regulatescardiac pages 8-9, paavola2020vezf1regulatescardiac pages 9-11)

In neonatal rat cardiomyocytes, VEZF1 silencing significantly altered 1,144 transcripts at FDR <0.05; 28 were increased and 53 decreased by more than twofold. Enrichment implicated muscle contraction and DCM pathways. Zebrafish Vezf1 knockdown reduced ventricular-myosin-heavy-chain expression by 92% and impaired the stress-induced increase in ejection performance without changing calcium-transient kinetics. These findings argue for altered contractile-gene transcription rather than a primary calcium-handling defect. (paavola2020vezf1regulatescardiac pages 5-7, paavola2020vezf1regulatescardiac pages 7-8, paavola2020vezf1regulatescardiac pages 8-9)

Promoter experiments showed that VEZF1 knockdown reduced β-MHC reporter activity by 52–80%. VEZF1 co-immunoprecipitated with TEAD1, and an MCAT element in the MYH7 promoter partly mediated the response. (paavola2020vezf1regulatescardiac pages 7-8, paavola2020vezf1regulatescardiac pages 9-11, paavola2020vezf1regulatescardiac pages 11-12)

Vascular and epigenetic dimensions

VEZF1 also regulates vasculogenesis and angiogenesis. Zebrafish knockdown altered axial-vessel geometry and stress-induced intersegmental-vessel formation. Endothelial signaling may therefore contribute, but cardiomyocyte-autonomous effects are supported by isolated-cell experiments. (paavola2020vezf1regulatescardiac pages 4-5, paavola2020vezf1regulatescardiac pages 11-12)

VEZF1 has previously been implicated in regulation of DNMT3B and DNA methylation, but no DCM100-specific epigenomic signature has been demonstrated. Likewise, no disease-specific proteomic, metabolomic, lipidomic, single-cell, spatial-transcriptomic, or CRISPR-screen dataset was found.

Suggested ontology annotations

• GO biological process: regulation of DNA-templated transcription; cardiac muscle contraction; regulation of heart contraction; cardiac muscle-cell development; angiogenesis; response to adrenergic stimulus.
• GO cellular component: nucleus (GO:0005634), transcription-regulator complex, sarcomere (GO:0030017) downstream.
• Cell Ontology: cardiomyocyte (CL:0002494), ventricular cardiomyocyte, endothelial cell (CL:0000115), cardiac fibroblast as a downstream remodeling cell.

7. Anatomical structures affected

The primary organ is the heart (UBERON:0000948), particularly myocardium (UBERON:0002084) and left ventricle (UBERON:0002080). Cardiomyocytes are the principal effector cells; cardiac endothelial cells may contribute through vascular and paracrine regulation. VEZF1 acts in the nucleus, while downstream damage involves sarcomeres and the contractile apparatus. (paavola2020vezf1regulatescardiac pages 1-2, paavola2020vezf1regulatescardiac pages 9-11, paavola2020vezf1regulatescardiac pages 11-12)

Secondary involvement in advanced DCM can include lungs, liver, kidneys, and systemic venous tissues through low cardiac output and congestion. These are complications of heart failure, not primary VEZF1 target organs. Lateralization is not applicable.

8. Temporal development

The DCM100-specific onset distribution is unknown. Generic inherited DCM may be clinically silent before progressive LV enlargement, reduced systolic function, symptomatic heart failure, arrhythmia, or sudden death. In genetic DCM, ventricular enlargement may precede measurable functional decline, and strain abnormalities may precede dimensional changes in relatives. (mcnally2017dilatedcardiomyopathygenetic pages 2-3)

A practical course model is:

1. genotype-positive/phenotype-negative;
2. subtle strain or ECG abnormality;
3. LV enlargement with mild systolic dysfunction;
4. symptomatic DCM/HFrEF;
5. advanced heart failure, malignant arrhythmia, mechanical support, or transplantation.

Spontaneous or treatment-associated reverse remodeling occurs in generic DCM, but no remission rate or critical intervention window is known for DCM100.

9. Inheritance and population

The available human evidence supports familial autosomal-dominant inheritance. Each child of a heterozygous carrier would therefore have a theoretical 50% transmission probability, although disease penetrance may be incomplete or age-dependent. Actual DCM100 penetrance and expressivity have not been quantified.

No subtype-specific prevalence, incidence, carrier frequency, founder effect, ethnic enrichment, geographic distribution, sex ratio, or age distribution is known. DCM100 should presently be considered ultra-rare. In DCM overall, familial disease is estimated in approximately 30–50% of cases, and an identifiable genetic cause is found in roughly 40% of familial cases; these values must not be assigned to VEZF1 specifically. (mcnally2017dilatedcardiomyopathygenetic pages 2-3)

10. Diagnostics

Clinical evaluation

The phenotype should be established independently of genotype through:

• history, three-generation pedigree, physical examination, and exclusion of ischemic/loading causes;
• 12-lead ECG and ambulatory monitoring for conduction disease and atrial/ventricular arrhythmia;
• transthoracic echocardiography for LV dimensions, ejection fraction, fractional shortening, valve regurgitation, and strain;
• cardiac MRI for chamber volumes, function, edema, and fibrosis/late gadolinium enhancement;
• BNP or NT-proBNP and troponin as severity/injury markers;
• laboratory exclusion of thyroid, metabolic, infectious, inflammatory, toxic, and nutritional causes where clinically indicated. CMR fibrosis has prognostic value in broader DCM. (mcnally2017dilatedcardiomyopathygenetic pages 2-3)

Endomyocardial biopsy is not routine for genetic DCM but may be appropriate when myocarditis, infiltrative disease, storage disease, or a treatment-changing inflammatory diagnosis is suspected.

Genetic testing

A contemporary strategy is a validated cardiomyopathy panel with deletion/duplication analysis, ensuring VEZF1 coverage if the laboratory recognizes the gene–disease relationship. Exome or genome sequencing is appropriate when panel testing is negative, especially in multiplex families; RNA studies may clarify splice variants. A VUS must not be used for predictive testing or irreversible management decisions.

Once a pathogenic familial variant is confirmed, offer targeted cascade testing to first-degree relatives. Genotype-positive relatives require longitudinal ECG and imaging surveillance. If the causal variant remains uncertain, first-degree relatives should still receive phenotype screening because familial DCM may be clinically silent. (mcnally2017dilatedcardiomyopathygenetic pages 2-3)

CMA, karyotyping, FISH, mitochondrial-genome testing, and repeat-expansion testing are not first-line for isolated DCM100 unless syndromic findings suggest another diagnosis.

Differential diagnosis

Exclude ischemic cardiomyopathy, myocarditis, tachycardia-induced cardiomyopathy, toxic/alcohol-related disease, peripartum cardiomyopathy, endocrine/nutritional disease, mitochondrial/metabolic cardiomyopathy, neuromuscular disease, congenital heart disease, and other genetic DCM genes such as TTN, LMNA, FLNC, DSP, RBM20, BAG3, and PLN.

11. Outcome and prognosis

No DCM100-specific survival, transplant-free survival, sudden-death rate, recovery rate, or validated prognostic biomarker is available. Prognosis should therefore be based on the observed phenotype rather than the VEZF1 label alone.

Generic adverse markers include severe LV dysfunction or dilatation, persistent symptoms, ventricular arrhythmia, conduction disease, syncope, fibrosis on CMR, severe mitral regurgitation, rising natriuretic peptides, and failure to reverse remodel. DCM can lead to chronic disability, recurrent hospitalization, thromboembolism, progressive pump failure, ventricular arrhythmia, sudden cardiac death, ventricular-assist-device implantation, or transplantation. Disease-specific quality-of-life statistics are unavailable.

12. Treatment

There is no approved VEZF1-targeted therapy, gene therapy, RNA therapy, or DCM100-specific clinical trial. Treatment is phenotype-directed and extrapolated from DCM/HFrEF practice:

• neurohormonal heart-failure therapy appropriate to age and physiology: ACE inhibitor/ARB or ARNI, evidence-based β-blocker, mineralocorticoid-receptor antagonist, and an SGLT2 inhibitor in eligible patients;
• loop diuretic for congestion;
• anticoagulation only for standard indications such as atrial fibrillation, intracardiac thrombus, or embolism—not solely for the genotype;
• antiarrhythmic therapy, catheter ablation, or pacing where indicated;
• ICD for guideline-defined sudden-death prevention and CRT for qualifying ventricular dysfunction/electrical dyssynchrony;
• temporary or durable mechanical circulatory support and heart transplantation for refractory advanced failure.

Pediatric prescribing requires specialist dosing and recognition that much evidence is extrapolated from adults. No pharmacogenomic interaction with VEZF1 is known.

Suggested NCIt concepts include heart-failure therapy, beta-adrenergic blocking agent therapy, angiotensin-receptor/neprilysin inhibitor therapy, diuretic therapy, implantable cardioverter-defibrillator placement, cardiac resynchronization therapy, ventricular-assist-device therapy, and heart transplantation.

Experimental cell therapies investigated in generic nonischemic DCM cannot be considered DCM100 treatment. ClinicalTrials.gov searches identified broad pediatric/DCM studies, but none selected patients by VEZF1 genotype.

13. Prevention

Primary prevention

The inherited variant itself cannot currently be prevented after conception. Avoidance of cardiotoxins and treatment of hypertension, arrhythmia, infection, endocrine disease, and other myocardial stressors are prudent but unproven as VEZF1-specific preventive measures.

Secondary prevention

The most actionable intervention is family identification and surveillance: genetic counseling, cascade testing for a confirmed pathogenic variant, periodic ECG/ambulatory monitoring and echocardiography or CMR, and early treatment of ventricular dysfunction. Reproductive options may include prenatal diagnosis or preimplantation genetic testing once a clearly pathogenic familial variant is established.

Tertiary prevention

Guideline-directed heart-failure therapy, rhythm surveillance, vaccination according to routine schedules, exercise counseling, prompt management of decompensation, and devices when indicated aim to prevent hospitalization, embolism, sudden death, and end-stage failure. There is no DCM100-specific immunization or chemoprophylaxis.

14. Other species and natural disease

No naturally occurring VEZF1-related DCM100 has been established in companion animals, livestock, or wildlife, and no breed-specific VBO annotation is justified. The disorder is not infectious and has no zoonotic or cross-species transmission.

Relevant experimental taxa are Homo sapiens (NCBI Taxon 9606), Mus musculus (10090), Rattus norvegicus (10116), and Danio rerio (7955). VEZF1 function is evolutionarily conserved across vertebrates. (paavola2020vezf1regulatescardiac pages 1-2)

15. Model organisms and advanced research

Zebrafish

Morpholino-mediated Vezf1 depletion produced reduced cardiomyocyte growth, pericardial enlargement, vascular abnormalities, and impaired β-adrenergic augmentation of contractility. Co-injection of Vezf1 mRNA rescued vascular phenotypes, supporting knockdown specificity. Calcium-transient kinetics were preserved, while ventricular MHC expression fell markedly. Limitations include transient morpholino knockdown, embryonic physiology, and absence of the exact human allele. (paavola2020vezf1regulatescardiac pages 4-5, paavola2020vezf1regulatescardiac pages 5-7, paavola2020vezf1regulatescardiac pages 8-9)

Rodent cardiomyocytes and mice

VEZF1 knockdown in neonatal and adult rat ventricular cardiomyocytes reduced cell growth, shortening, MYH7/β-MHC expression, and β-MHC promoter activity; it increased skeletal α-actin and altered the contractile transcriptome. These experiments support a cardiomyocyte-autonomous transcriptional mechanism. (paavola2020vezf1regulatescardiac pages 5-7, paavola2020vezf1regulatescardiac pages 7-8, paavola2020vezf1regulatescardiac pages 9-11)

Vezf1-null mice are embryonically lethal with major vascular defects, making a conventional null model unsuitable for adult DCM natural history. A conditional cardiomyocyte-specific knock-in of the human DCM100 variant would be more informative. (paavola2020vezf1regulatescardiac pages 2-3)

Human tissues

Across two human heart-failure expression datasets, VEZF1 expression was approximately 20–25% lower in idiopathic cardiomyopathy and 16–25% lower in ischemic cardiomyopathy than controls. In a separate autopsy series, expression was 43% lower in ischemic-heart-disease sudden-death hearts. These observations show association with diseased myocardium but do not prove that acquired reduction causes DCM100. (paavola2020vezf1regulatescardiac pages 4-5)

Priority research needs

1. Independent VEZF1 families and rigorous ClinGen-level replication.
2. Public deposition and expert classification of the defining variant.
3. Longitudinal penetrance and genotype–phenotype studies.
4. Patient-derived iPSC cardiomyocytes and isogenic correction.
5. Variant-specific knock-in mouse or zebrafish models.
6. Single-cell and spatial transcriptomics separating cardiomyocyte from endothelial effects.
7. ChIP-seq/CUT&RUN mapping of VEZF1–TEAD1 targets.
8. Rescue studies testing whether restoration of VEZF1 or MYH7 normalizes contractility.

Key abstract quotations and source appraisal

• The 2020 mechanistic paper states: “We demonstrate a role for Vezf1 in regulation of compensatory cardiac growth and cardiomyocyte contractile function.” This is supported by zebrafish and cultured-cell experiments, not by a DCM100 clinical cohort. (paavola2020vezf1regulatescardiac pages 1-2)
• Its principal mechanistic finding was that VEZF1 knockdown regulates contraction/DCM-related genes and identifies MYH7/β-MHC as a key target, with TEAD1 as a binding partner. (paavola2020vezf1regulatescardiac pages 1-2, paavola2020vezf1regulatescardiac pages 7-8)
• The defining 2023 human paper is titled “VEZF1 loss-of-function mutation underlying familial dilated cardiomyopathy.” Its PMID and disease–gene linkage are verified, but exact abstract wording and patient-level data were not recoverable in the accessible corpus. (OpenTargets Search: Cardiomyopathy Dilated 100)

Overall interpretation

DCM100 is best regarded as a provisional-to-emerging, ultra-rare VEZF1-associated autosomal-dominant DCM subtype supported by one familial report and biologically coherent experimental evidence. VEZF1 connects endothelial biology with cardiomyocyte transcription, particularly the TEAD1–MYH7 contractile program. Nevertheless, the present evidence does not justify subtype-specific estimates of penetrance, prognosis, variant frequency, or treatment response. Clinical care should therefore combine confirmation of the familial molecular finding with standard hereditary-DCM phenotyping, cascade screening, longitudinal surveillance, and guideline-directed heart-failure and arrhythmia management. (OpenTargets Search: Cardiomyopathy Dilated 100, paavola2020vezf1regulatescardiac pages 1-2, mcnally2017dilatedcardiomyopathygenetic pages 2-3)

References

1. (OpenTargets Search: Cardiomyopathy Dilated 100): Open Targets Query (Cardiomyopathy Dilated 100, 6 results). Buniello, A. et al. (2025). Open Targets Platform: facilitating therapeutic hypotheses building in drug discovery. Nucleic Acids Research.

2. (paavola2020vezf1regulatescardiac pages 1-2): Jere Paavola, Tarja Alakoski, Johanna Ulvila, Teemu Kilpiö, Juuso Sirén, Sanni Perttunen, Suneeta Narumanchi, Hong Wang, Ruizhu Lin, Katja Porvari, Juhani Junttila, Heikki Huikuri, Katariina Immonen, Päivi Lakkisto, Johanna Magga, Ilkka Tikkanen, and Risto Kerkelä. Vezf1 regulates cardiac structure and contractile function. EBioMedicine, 51:102608, Jan 2020. URL: https://doi.org/10.1016/j.ebiom.2019.102608, doi:10.1016/j.ebiom.2019.102608. This article has 22 citations and is from a peer-reviewed journal.

3. (paavola2020vezf1regulatescardiac pages 5-7): Jere Paavola, Tarja Alakoski, Johanna Ulvila, Teemu Kilpiö, Juuso Sirén, Sanni Perttunen, Suneeta Narumanchi, Hong Wang, Ruizhu Lin, Katja Porvari, Juhani Junttila, Heikki Huikuri, Katariina Immonen, Päivi Lakkisto, Johanna Magga, Ilkka Tikkanen, and Risto Kerkelä. Vezf1 regulates cardiac structure and contractile function. EBioMedicine, 51:102608, Jan 2020. URL: https://doi.org/10.1016/j.ebiom.2019.102608, doi:10.1016/j.ebiom.2019.102608. This article has 22 citations and is from a peer-reviewed journal.

4. (paavola2020vezf1regulatescardiac pages 7-8): Jere Paavola, Tarja Alakoski, Johanna Ulvila, Teemu Kilpiö, Juuso Sirén, Sanni Perttunen, Suneeta Narumanchi, Hong Wang, Ruizhu Lin, Katja Porvari, Juhani Junttila, Heikki Huikuri, Katariina Immonen, Päivi Lakkisto, Johanna Magga, Ilkka Tikkanen, and Risto Kerkelä. Vezf1 regulates cardiac structure and contractile function. EBioMedicine, 51:102608, Jan 2020. URL: https://doi.org/10.1016/j.ebiom.2019.102608, doi:10.1016/j.ebiom.2019.102608. This article has 22 citations and is from a peer-reviewed journal.

5. (paavola2020vezf1regulatescardiac pages 11-12): Jere Paavola, Tarja Alakoski, Johanna Ulvila, Teemu Kilpiö, Juuso Sirén, Sanni Perttunen, Suneeta Narumanchi, Hong Wang, Ruizhu Lin, Katja Porvari, Juhani Junttila, Heikki Huikuri, Katariina Immonen, Päivi Lakkisto, Johanna Magga, Ilkka Tikkanen, and Risto Kerkelä. Vezf1 regulates cardiac structure and contractile function. EBioMedicine, 51:102608, Jan 2020. URL: https://doi.org/10.1016/j.ebiom.2019.102608, doi:10.1016/j.ebiom.2019.102608. This article has 22 citations and is from a peer-reviewed journal.

6. (mcnally2017dilatedcardiomyopathygenetic pages 2-3): Elizabeth M. McNally and Luisa Mestroni. Dilated cardiomyopathy: genetic determinants and mechanisms. Circulation Research, 121:731–748, Sep 2017. URL: https://doi.org/10.1161/circresaha.116.309396, doi:10.1161/circresaha.116.309396. This article has 995 citations and is from a highest quality peer-reviewed journal.

7. (paavola2020vezf1regulatescardiac pages 8-9): Jere Paavola, Tarja Alakoski, Johanna Ulvila, Teemu Kilpiö, Juuso Sirén, Sanni Perttunen, Suneeta Narumanchi, Hong Wang, Ruizhu Lin, Katja Porvari, Juhani Junttila, Heikki Huikuri, Katariina Immonen, Päivi Lakkisto, Johanna Magga, Ilkka Tikkanen, and Risto Kerkelä. Vezf1 regulates cardiac structure and contractile function. EBioMedicine, 51:102608, Jan 2020. URL: https://doi.org/10.1016/j.ebiom.2019.102608, doi:10.1016/j.ebiom.2019.102608. This article has 22 citations and is from a peer-reviewed journal.

8. (paavola2020vezf1regulatescardiac pages 4-5): Jere Paavola, Tarja Alakoski, Johanna Ulvila, Teemu Kilpiö, Juuso Sirén, Sanni Perttunen, Suneeta Narumanchi, Hong Wang, Ruizhu Lin, Katja Porvari, Juhani Junttila, Heikki Huikuri, Katariina Immonen, Päivi Lakkisto, Johanna Magga, Ilkka Tikkanen, and Risto Kerkelä. Vezf1 regulates cardiac structure and contractile function. EBioMedicine, 51:102608, Jan 2020. URL: https://doi.org/10.1016/j.ebiom.2019.102608, doi:10.1016/j.ebiom.2019.102608. This article has 22 citations and is from a peer-reviewed journal.

9. (paavola2020vezf1regulatescardiac pages 9-11): Jere Paavola, Tarja Alakoski, Johanna Ulvila, Teemu Kilpiö, Juuso Sirén, Sanni Perttunen, Suneeta Narumanchi, Hong Wang, Ruizhu Lin, Katja Porvari, Juhani Junttila, Heikki Huikuri, Katariina Immonen, Päivi Lakkisto, Johanna Magga, Ilkka Tikkanen, and Risto Kerkelä. Vezf1 regulates cardiac structure and contractile function. EBioMedicine, 51:102608, Jan 2020. URL: https://doi.org/10.1016/j.ebiom.2019.102608, doi:10.1016/j.ebiom.2019.102608. This article has 22 citations and is from a peer-reviewed journal.

10. (paavola2020vezf1regulatescardiac pages 2-3): Jere Paavola, Tarja Alakoski, Johanna Ulvila, Teemu Kilpiö, Juuso Sirén, Sanni Perttunen, Suneeta Narumanchi, Hong Wang, Ruizhu Lin, Katja Porvari, Juhani Junttila, Heikki Huikuri, Katariina Immonen, Päivi Lakkisto, Johanna Magga, Ilkka Tikkanen, and Risto Kerkelä. Vezf1 regulates cardiac structure and contractile function. EBioMedicine, 51:102608, Jan 2020. URL: https://doi.org/10.1016/j.ebiom.2019.102608, doi:10.1016/j.ebiom.2019.102608. This article has 22 citations and is from a peer-reviewed journal.

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