Keshan disease

Summary

Keshan disease (MONDO:0000241) is a disease. A subtype of cardiomyopathy — broader associated-gene and molecular evidence is on the parent page (see Disease family below).

Clinical features

No curated clinical features (Orphanet) for this disease.

Identifiers

Disease identifiers

Field	Value
Canonical name	Keshan disease
Mondo ID	MONDO:0000241
MeSH	C536166
DOID	DOID:0050083
ICD-11	1307765114
SNOMED CT	46939000
UMLS	C0268095
MedGen	78639
GARD	0008761
Is cancer (heuristic)	no

Also known as: congestive cardiomyopathy due to selenium deficiency · enlarged heart and poor heart function

Disease family

This is a subtype of cardiomyopathy. Genetic, therapeutic, and trial evidence is largely curated at the broader-term level — see the parent page for the associated-gene cohort and molecular evidence.

Classification path: disease › human disease › disease by body system or component › musculoskeletal system disorder › muscle tissue disorder › cardiomyopathy › Keshan disease

Related subtypes (11): intrinsic cardiomyopathy, extrinsic cardiomyopathy, idiopathic cardiomyopathy, familial cardiomyopathy, non-compaction cardiomyopathy, Chagas cardiomyopathy, Uhl anomaly, Tako-tsubo cardiomyopathy, cardiomyopathy due to anthracyclines, doxorubicin induced cardiomyopathy, autoimmune cardiomyopathy

Genetics & variants

GWAS landscape

No GWAS associations recorded — common-variant (GWAS) studies don’t cover this disease (typical for Mendelian / rare diseases). See the curated gene cohort and Mendelian overlap below.

Variant details and genetic-evidence tiers

No tiered GWAS variants or ClinVar records for this disease.

Genes & proteins

No associated-gene cohort resolved for this disease. Atlas builds the molecular and therapeutic sections — associated genes, protein families, druggability, pathways, interactions, and drug associations — by aggregating over a disease’s associated genes (resolved via GWAS / GenCC / ClinVar / CIViC), and none resolved here. This is expected for antibody-mediated, autoimmune, or otherwise non-gene-defined conditions; the curated evidence for this disease is its clinical features, GWAS susceptibility, and clinical trials (above).

Function

No pathway enrichment — requires an associated-gene cohort.

Therapeutics

No druggable-target or therapeutic data for this disease’s cohort.

Clinical trials & evidence

Clinical trials

Clinical trials: 0.