CDKN2B gene expression is affected by 9p21.3 rs10757278 in CAD patients, six months after the MI

Chromatin accessibility and gene expression during adipocyte differentiation identify context-dependent effects at cardiometabolic GWAS loci

“…Of 16,076 total peaks linked to a gene through at least one of the three approaches (S12 Table ), 78 peaks were linked to the same gene through all three approaches and 5,145 peaks were linked to the same gene through two or more approaches (Fig 2E). Of the 78 peaks linked to 59 genes through all three approaches, interesting candidate regulatory elements include four peaks linked to CDKN2B, whose gene product has known roles in cell cycle control and whose regulation has been linked to coronary artery disease [36,37]. Of the 5,145 peaks linked to 1,670 genes through at least two approaches, 1,143 linked from preadipocyte-dependent peaks and 1,945 linked from adipocyte-dependent peaks (2,057 linked from other context-dependent peaks).…”

From multi-omics approaches to personalized medicine in myocardial infarction

“…Their findings demonstrated that lncRNA SNHG8 not only emerged as a risk factor for MI but also exhibited substantial diagnostic potential. Furthermore, extensive transcriptomic studies have revealed a significant correlation between the abnormal expression of inflammation-related genes, such as VEGFA ( 102 ), TNF ( 103 ), IL6 ( 103 , 104 ), IL6R ( 104 ), PTGS2 ( 105 ), immune response-related genes including CDKN2B ( 106 ), CDKN1C ( 107 ), TLR2 ( 108 ), TLR4 ( 108 ), apoptosis and proliferation-related genes like F3 ( 109 ), BTG2 ( 110 ), TXNIP ( 111 ), SAMSN1 ( 112 ), lipid metabolism-related genes such as PPARGC1A ( 113 ), ACSL1 ( 114 ), ABCG1 ( 115 ), SULT2B1 ( 116 ), and extracellular matrix (ECM) and collagen-related genes, such as MMP2 ( 117 ), MMP9 ( 117 ), LTBP4 ( 118 ), TNXB ( 118 ), and the occurrence and development of MI. These findings offer crucial insights into a deeper comprehension of the mechanisms underlying MI and hold promise for the development of more precise approaches for preventing and treating heart disease in the future.…”

Αναζήτηση Βιοδεικτών Σε Ασθενείς Με Επαναλαμβανόμενα Καρδιαγγειακά Περιστατικά Για Την Βέλτιστη Κλινική Πρακτική

“…Πολλές GWAS μελέτες, καθώς και μετα-αναλύσεις σε μια σειρά πληθυσμούς (αν και πρωτίστως στον πληθυσμό των Ευρωπαίων Καυκασίων, CEU) έχουν συσχετίσει τη χρωμοσωμική περιοχή 9p21.3 με τη προδιάθεση για καρδιαγγειακά περιστατικά, κυρίως τη στεφανιαία νόσο και το έμφραγμα του μυοκαρδίου, αλλά και την επανενεργοποίηση των αιμοπεταλίων (Yamada and Yasukochi, 2018). Η περιοχή 9p21.3 είναι πλούσια σε ενισχυτές και ογκο-κατασταλτικά γονίδια (Zivotić et al,2019). Σε αυτήν, εντοπίζονται τα γονίδια που κωδικοποιούν δύο αναστολείς κινασών που εξαρτώνται από την κυκλίνη (cyclin-dependent kinase inhibitors, CDKN2A και CDKN2B).…”