Cardio Lab · DeCure for X

DeCure for Cardiomyopathy, dilated, 2F

DeCure's autonomous Cardio AI scientist is researching a drug-repurposing hypothesis for cardiomyopathy, dilated, 2F — screening already-approved drugs against its 1-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.

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The disease map

Disease moduleCardiomyopathy, dilated, 2F maps to a 1-gene Open Targets module — the target space DeCure's AI scientist screens approved drugs against.
DeCure.ai methodSignature reversal (LINCS) plus network proximity (STRING) rank already-approved drugs likely to perturb this module — the same engine that produces DeCure.ai's repurposing hypotheses.
Repurposing thesisScreening approved medicines against this disease module, then publishing the evidence for the strongest candidate. Known pharmacology and human exposure data make the first question sharper — they do not establish safety or efficacy in a new indication.

Research record

01
ResearchComing soon
Candidate research + dossier — target rationale, drug-repurposing thesis and evidence pack.proof: Published dossier + on-chain hash
02
ValidationComing soon
In-vitro biological validation at a contract research org (CRO).proof: CRO contract + in-vitro report
03
Peer review & paperComing soon
Peer-reviewed paper published open-access (preprint + journal).proof: DOI + open-access link + on-chain hash

Current lead

No approved-drug candidate for cardiomyopathy, dilated, 2f is corroborated in the literature DeepSearch retrieved. Some conditions are managed with non-pharmacological care — a device, surgery or physical therapy — rather than a medicine; that may be the case here, or the literature we found may simply be too sparse yet to support a drug-repurposing angle.

Molecular view

BAG cochaperone 5 (BAG5)BAG5 is one of the genes genetically linked to this disease in Open Targets — shown as context, not as a drug target we're pursuing: no approved-drug candidate for this disease is yet corroborated in the literature we found.

Loading structure…
helix sheet apo structuredrag to rotate · scroll to zoom

RCSB Protein Data Bank · entry 3A8Y · 2.3 Å · ligand none (apo structure). Experimental structure, not a prediction.

What the evidence adds up to

Idiopathic dilated cardiomyopathy remains a condition whose origins are not fully understood, and clinicians continue to face challenges in identifying and treating its causes to improve symptoms and survival. Causative genetic mutations have been identified in more than 40 genes encoding proteins belonging to different cellular structures and pathways, including genes for contractile proteins, Z‑disks, cytoskeletons, desmosomes, and ion channels. The LMOD2 gene has been demonstrated to be closely associated with the pathogenesis of DCM; in 2024 a heterozygous LMOD2 knockout human embryonic stem cell line was established using the CRISPR/Cas9 system to provide a DCM cell model for further research.

In a 2009 study of 20 patients with dilated cardiomyopathy (10 ischemic, 10 idiopathic) who received the Acorn CorCap cardiac support device, all patients survived surgery but four died during a mean follow-up of 32 months. After surgery there was a significant reduction in cardiac dimensions, improved functional capacity, and improved quality of life, with no significant differences between ischemic and idiopathic patients. The authors concluded the device was safe and simple but called for further studies to identify optimal patient selection criteria and timing of surgery, and to assess long-term effects.

A 2014 case report described a patient who underwent orthotopic transplantation of a putrid heart along with medication, which the authors said improved quality of life and prognosis. A 2023 review noted that heart failure remains a leading cause of morbidity and mortality globally, and that even after diagnosis of dilated cardiomyopathy only 25% to 40% of patients receive guideline-directed medical therapy. A 2025 review argued for further introduction of genetic testing into clinical practice for personalised management and timely identification of risk factors in family members at the pre‑nosological stage.

What is still missing are large, long-term randomised trials comparing any of these interventions against standard medical therapy alone, validated criteria for selecting which patients might benefit from surgical containment devices, and prospective studies that stratify patients by the specific genetic mutations now known to underlie the disease. The heterogeneity of dilated cardiomyopathy means that no single approach has been proven to alter the natural history of the condition in a broad unselected population.

Evidence

Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.

Cleveland Clinic Journal of Medicine · 2002 · 44 citations

Idiopathic dilated cardiomyopathy: a common but mystifying cause of heart failure.

AbstractWhile researchers try to elucidate the origins of idiopathic dilated cardiomyopathy, clinicians continue to face the challenges of identifying and treating the causes of this condition to improve symptoms and survival. We review classification schemes for dilated cardiomyopathy and the current range of diagnostic and therapeutic options and treatment goals.

https://doi.org/10.3949/ccjm.69.6.481
Journal of Cardiovascular Medicine · 2016 · 15 citations

Genetic bases of dilated cardiomyopathy

AbstractCardiomyopathies represent a wide and heterogeneous group of diseases wherein a genetic cause has been consistently identified.Dilated cardiomyopathy (DCM) is characterized by ventricular dilation and progressive systolic dysfunction, and it is the most common form of cardiomyopathy.Causative genetic mutations have been identified in more than 40 genes encoding proteins belonging to different cellular structures and pathways.A great diversity of pathways has been implied in the pathogenesis of DCM, depending on the affected genes and on the dislodged intracellular structures or mechanisms.This review describes the major genes and focus on the pathophysiologic mechanisms of DCM, with a special consideration of the most recent discoveries in the field.

https://doi.org/10.2459/jcm.0000000000000432
Journal of Cardiac Surgery · 2009 · 10 citations

Midterm Results of Passive Containment Surgery Using the Acorn Cor Cap⢠Cardiac Support Device in Dilated Cardiomyopathy

AbstractBACKGROUND AND AIM: To evaluate the echocardiographic, functional, and quality of life improving effects of passive containment surgery using the CorCap cardiac support device (CSD; Acorn Cardiovascular Inc., St. Paul, MN, USA) in patients with dilated cardiomyopathy and to investigate the possible differences in ischemic versus idiopathic (i.e., normal angiograms) cardiomyopathy. METHODS: Twenty patients with dilated cardiomyopathy (10 with ischemic and 10 with idiopathic disease) were subjected to application of the cardiac support device, between June 2001 and October 2006. Preoperatively and at follow-up cardiac dimensions, cardiac function, functional capacity, and quality of life were evaluated. Follow-up is complete with a mean follow-up time of 32 +/- 5 months. RESULTS: All patients survived the surgery; four patients died during the follow-up time. Following surgery, there was a significant reduction in cardiac dimensions, improved functional capacity, and improved quality of life. No significant differences could be seen between patients with ischemic versus idiopathic disease. CONCLUSION: Application of the CSD is safe and simple in patients with dilated cardiomyopathy and without any apparent negative effects. Further studies are needed to identify optimal patient selection criteria as well as optimal timing of surgery and to assess the long-term effects of this treatment.

https://doi.org/10.1111/j.1540-8191.2008.00771.x
Journal of clinical practice · 2014 · 2 citations · open access

MODERN APPROACH TO MANAGEMENT OF DILATED CARDIOMYOPATHY: CASE REPORT

AbstractDescription of case reports of a patient with diagnosis of dilated cardiomyopathy granting of a historical reference and modern ideas about the etiology, pathogenesis, course, and management of the disease. Performed surgical treatment (orthotopic transplantation of putrid heart), along with medication, allowed to improve the quality of life and prognosis of the disease.

https://doi.org/10.17816/clinpract5117-25
Heart failure journal of India · 2023 · 0 citations · open access

Management of non-ischemic dilated cardiomyopathy

AbstractHeart failure (HF) remains a leading cause of morbidity and mortality globally. For every 23 s, a new case of HF is diagnosed in India. Dilated cardiomyopathy is characterized by dilatation of the left ventricle or both ventricles with impaired function, which cannot be fully explained by abnormal loading conditions or coronary artery disease. The heterogeneity in etiology and clinical presentation of dilated cardiomyopathy makes timely diagnosis and treatment challenging. Even after diagnosis, only 25%–40% receive guideline-directed medical therapy.

https://doi.org/10.4103/hfji.hfji_1_22
Ukrainian Therapeutical Journal · 2025 · 0 citations · open access

Clinical and genetic heterogeneity of dilated cardiomyophathy. Review

AbstractThis article contains an overview of published scientific sources from the MEDLINE database on the PubMed, Web of Science, Scopus platforms regarding the dilated cardiomyopathy with an emphasis on clinical and genetic aspects. Taking into account the etiological origins, various classification categories of myocardial damages are presented — non‑syndromic, acquired (secondary), syndromic cardiomyopathies. The modern definition of dilated cardiomyophaty is presented in accordance with the recommendations of international experts. The review focuses on cardiomyocyte components that are important for energy generation and transmission, mechanical and signaling functions, and maintenance of electrolyte homeostasis. A list of genes encoding contractile proteins and their regulatory elements in components of sarcomeres, Z‑disks, cytoskeletons, desmosomes, and ion channels of cardiomyocytes is provided. The role of pathogenic gene variants associated with mechanisms contributing to the initiation, clinical manifestation, and prognosis of dilated cardiomyopathy is summarized. The causal relationships of mutations in the relevant genes with various clinical scenarios of dilated cardiomyopathy are shown: onset of the diseases, structural myocardial disorders, arrhythmogenic complications, and progression of heart failure. Genetic analysis has become a stimulus for enriching the classification spectrum of cardiomyopathies through the creation of new terms. Specific forms of cardiomyophaties include desmosomal‑dependent cardiomyophathy, desmoplakin cardiomyophathy, RBM20 cardiomyophathy, and others. The argumentation for the further introduction of genetic testing into clinical practice is underlined for the purpose of personalized management of patients with cardiomyopathies and timely identification of risk factors for the disease in their family members at the pre‑nosological stage.

https://doi.org/10.30978/utj2025-3-48
Stem Cell Research · 2024 · 0 citations · open access

Establishment of heterozygous LMOD2 knockout human embryonic stem cell line (ZZUNEUi022-A-1) using CRISPR/Cas9 system

AbstractDilated Cardiomyopathy (DCM), a prevalent form of cardiomyopathy, is characterized by ventricular dilation and systolic dysfunction. Its etiology is intricate, encompassing multiple genetic and environmental elements. The LMOD2 (Leiomodin 2) gene has been demonstrated to be closely associated with the pathogenesis of DCM. In this study, a pure cell line was generated by knocking out the LMOD2 gene, and a DCM cell model was established through induced differentiation, thus providing a powerful experimental approach for further understanding the pathogenesis of DCM. It also provides a potential research orientation for the early diagnosis and individualized treatment of DCM.

https://doi.org/10.1016/j.scr.2024.103586

Disease module: DeepOracle (Open Targets). Structures: RDKit from PubChem SMILES. Literature: retrieved by DeepSearch across 234,678,978 indexed works (targeted per-candidate search), resolved on OpenAlex.

DeCure is a research and publication project, not medical advice and not a treatment. "DeCure for X" describes a research goal, not a claim that a cure exists. Backing a cure is a contribution to fund the research — it is not an investment, and confers no yield, royalty, equity or IP ownership. Papers are published open-access by the DeCure.ai DAO.