Unravelling convergent signaling mechanisms underlying the aging-disease nexus using computational language analysis

Junyent, Marina; Noori, Haki; De Schepper, Robin; Frajdenberg, Shanna; Khalid Abdullah Hussen Elsaigh, Razan; McDonald, Patricia H.; Duckett, Derek; Maudsley, Stuart

doi:http://dx.doi.org/10.3390/cimb47030189

Unravelling convergent signaling mechanisms underlying the aging-disease nexus using computational language analysis

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Junyent M, Noori H, De Schepper R, Frajdenberg S, Khalid Abdullah Hussen Elsaigh R, McDonald PH, Duckett D, Maudsley S. Unravelling convergent signaling mechanisms underlying the aging-disease nexus using computational language analysis. Curr Issues Mol Biol. 2025 Mar 14;47(3):189. DOI: 10.3390/cimb47030189

Abstract

Multiple lines of evidence suggest that multiple pathological conditions and diseases that account for the majority of human mortality are driven by the molecular aging process. At the cellular level, aging can largely be conceptualized to comprise the progressive accumulation of molecular damage, leading to resultant cellular dysfunction. As many diseases, e.g., cancer, coronary heart disease, Chronic obstructive pulmonary disease, Type II diabetes mellitus, or chronic kidney disease, potentially share a common molecular etiology, then the identification of such mechanisms may represent an ideal locus to develop targeted prophylactic agents that can mitigate this disease-driving mechanism. Here, using the input of artificial intelligence systems to generate unbiased disease and aging mechanism profiles, we have aimed to identify key signaling mechanisms that may represent new disease-preventing signaling pathways that are ideal for the creation of disease-preventing chemical interventions. Using a combinatorial informatics approach, we have identified a potential critical mechanism involving the recently identified kinase, Dual specificity tyrosine-phosphorylation-regulated kinase 3 (DYRK3) and the epidermal growth factor receptor (EGFR) that may function as a regulator of the pathological transition of health into disease via the control of cellular fate in response to stressful insults.