ArticleMolecular biology reports2025
Genetic variants in HSP40 co-chaperones modulate ischemic heart disease risk.
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Genetic Variants in HSP70 Family and BAG Co-Chaperone Genes: Associations with Coronary Artery Disease Risk and Potential Regulatory Effects.International journal of molecular sciences · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe chaperoning system, which is responsible for protein homeostasis, plays a significant role in cardiovascular diseases. Among molecular chaperones or heat shock proteins (HSPs), the HSP40 family, the main co-chaperone of HSP70, remains largely underexplored, especially in ischemic heart disease (IHD) risk. MATERIALS AND
resultsWe genotyped 834 IHD patients and 1,328 healthy controls for three SNPs (rs2034598 and rs7189628 DNAJA2 and rs4926222 DNAJB1) using probe-based real-time PCR. We observed that SNP rs7189628 DNAJA2 was associated with increased IHD risk in smokers (effect allele [EA] T, OR = 1.65, 95%CI 1.01-2.71, p = 0.036), while SNP rs2034598 DNAJA2 was associated with increased IHD risk in non-smokers (EA A, OR = 1.22, 95%CI 1.02-1.47, p = 0.036). Oppositely, SNP rs4926222 DNAJB1 was associated with reduced IHD risk in patients under 62 years old (EA G, OR = 0.73, 95%CI 0.54-0.98, p = 0.02). These SNPs also modulated clinical parameters: rs7189628 was associated with higher platelet counts in the entire group (p = 0.03) and males (p = 0.02), while rs2034598 was associated with lower platelet counts in the same groups accordingly (p = 0.03 and p = 0.047), earlier IHD onset in males (p = 0.03), and reduced activated partial thromboplastin time in smokers (p = 0.01); rs4926222 DNAJB1 was Linked to elevated prothrombin index in patients aged 62 and higher (p = 0.04) and lower BMI in smokers (p = 0.005) and males (p = 0.02).
conclusionOur findings suggest that genetic variants in the HSP40 family influence IHD risk and clinical features in a context-specific manner.
Indexed as
Identifiers
40928562What OpenQuestion holds
Registered trials
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.