Evidence map›Paper›PMID 42848261›Full record

ArticleMolecular biology reports2026

The relationship between coronary artery disease and the heat-resistant obscure chaperone Hero11.

Vladislav Shilenok, Ksenia Kobzeva, Olga Bushueva

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Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Vladislav ShilenokLaboratory of Genomic Research, Research Institute for Genetic and Molecular Epidemiology, Kursk State Medical University, Kursk, 305041, Russia.ORCID http://orcid.org/0000-0002-8400-6244
Ksenia KobzevaLaboratory of Genomic Research, Research Institute for Genetic and Molecular Epidemiology, Kursk State Medical University, Kursk, 305041, Russia.ORCID http://orcid.org/0000-0002-0652-2219
Olga BushuevaLaboratory of Genomic Research, Research Institute for Genetic and Molecular Epidemiology, Kursk State Medical University, Kursk, 305041, Russia. olga.bushueva@inbox.ru.ORCID http://orcid.org/0000-0003-3333-0623

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHeat-resistant obscure (Hero) proteins are a recently described class of intrinsically disordered proteins with chaperone-like activity. C19orf53 (Hero11) suppresses TDP-43 aggregation and is linked to mTORC1 signaling, suggesting a potential role in cellular pathways relevant to coronary artery disease (CAD). We investigated whether C19orf53 genetic variants are associated with CAD risk. METHODS AND

resultsWe genotyped seven C19orf53 single-nucleotide polymorphisms (SNPs) in 2,164 unrelated individuals of Russian ethnicity from Central Russia, including 836 patients with CAD and 1,328 controls. Associations with CAD risk and clinical traits were assessed using regression analyses with permutation correction, followed by functional annotation with bioinformatical resources. SNPs rs11666524 (effect allele [EA] A, OR = 1.21, 95% CI 1.02-1.45, p = 0.04) and rs2277947 (EA A, OR = 1.22, 95% CI 1.01-1.46, p = 0.03) were associated with increased CAD risk in the entire cohort. The strongest effects of C19orf53 SNPs were observed in subgroups without major CAD risk factors for: non-smokers (p = 0.02 for rs10104, rs11666524, and rs2277947); patients with normal fresh fruit/vegetable intake (p = 0.02 for rs10104, and rs346158; p = 0.016 for rs11666524, p = 0.007 for rs2277947, p = 0.04 for rs8107914); and in patients without obesity (p = 0.02 for rs10104, p = 0.01 for rs11666524, p = 0.004 for rs346157, p = 0.01 for rs2277947). Moreover, C19orf53 SNPs contribute to alterations in coagulation parameters.

conclusionsC19orf53 variants are associated with CAD susceptibility and coagulation-related traits, with effects modified by major lifestyle and metabolic risk factors.

Indexed as

Coronary Artery DiseaseAgedAllelesCase-Control StudiesFemaleGenetic Predisposition to DiseaseGenotypeHumansMaleMiddle AgedMolecular ChaperonesPolymorphism, Single NucleotideRisk FactorsRussiaMolecular ChaperonesC19orf53ChaperonesCoronary artery diseaseIntrinsically disordered proteinmTORC1

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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.