Shared Proteins and Pathways of Cardiovascular and Cognitive Diseases: Relation to Vascular Cognitive Impairment
Creators
- 1. Koc Univ, Grad Sch Sci & Engn, Computat Sci & Engn, TR-34450 Istanbul, Turkiye
- 2. Univ Pompeu Fabra, Dept Med & Life Sci, Lab Mol Physiol, Barcelona 08002, Spain
- 3. Univ Pompeu Fabra, Dept Med & Life Sci, Lab Struct Bioinformat GRIB, Barcelona 08002, Spain
- 4. Univ Pompeu Fabra, Dept Med & Life Sci, Lab Dynam Syst Biol, Barcelona 08002, Spain
- 5. Univ Tartu, Inst Comp Sci, EE-50090 Tartu, Estonia
- 6. Koc Univ, Dept Chem & Biol Engn, TR-34450 Istanbul, Turkiye
- 7. Koc Univ, Dept Comp Engn, TR-34450 Istanbul, Turkiye
Description
One of the primary goals of systems medicine is the detection of putative proteins and pathways involved in disease progression and pathological phenotypes. Vascular cognitive impairment (VCI) is a heterogeneous condition manifesting as cognitive impairment resulting from vascular factors. The precise mechanisms underlying this relationship remain unclear, which poses challenges for experimental research. Here, we applied computational approaches like systems biology to unveil and select relevant proteins and pathways related to VCI by studying the crosstalk between cardiovascular and cognitive diseases. In addition, we specifically included signals related to oxidative stress, a common etiologic factor tightly linked to aging, a major determinant of VCI. Our results show that pathways associated with oxidative stress are quite relevant, as most of the prioritized vascular cognitive genes and proteins were enriched in these pathways. Our analysis provided a short list of proteins that could be contributing to VCI: DOLK, TSC1, ATP1A1, MAPK14, YWHAZ, CREB3, HSPB1, PRDX6, and LMNA. Moreover, our experimental results suggest a high implication of glycative stress, generating oxidative processes and post-translational protein modifications through advanced glycation end-products (AGEs). We propose that these products interact with their specific receptors (RAGE) and Notch signaling to contribute to the etiology of VCI.
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