Mimicking Cell‐Death Process of Vertebrates Using Analog Electronics Circuit

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Abstract Apoptosis, traditionally regarded as a straightforward cell‐suicide process triggered by cellular stress, plays a vital role in development, immune function, and disease progression. This research presents a synthetic model of the intrinsic (mitochondrial) apoptosis pathway, focusing on programmed cell death initiated by severe DNA damage. Through an in vitro approach, the study quantitatively analyzes apoptotic behavior using mathematical formulations of key regulatory proteins, modeled with ordinary differential equations using Law of Mass Action. A comprehensive system model is developed to capture the full signaling cascade of apoptosis. Furthermore, a novel cytomorphic model is introduced, employing Metal Oxide Semiconductor (MOS) technology to simulate molecular dynamics by drawing parallels with electron flow in transistors. The analytical output of the model reveals time‐dependent protein activity profiles, accurately representing the distinct phases of apoptosis. Notably, simulations show a rapid rise in Caspase‐3 activity following an apoptotic trigger, consistent with its role as an executioner caspase. The electronic circuit model is validated against experimental data from cell culture studies, reinforcing its accuracy and biological relevance. Additionally, the hardware implementation of the apoptosis‐based cytomorphic system is realized using the NI myRIO 1900 tool, demonstrating practical feasibility and integration potential. These findings demonstrate that MOS‐based electronic analogs of apoptosis pathways can effectively mimic protein behavior, offering a faster, more cost‐effective, and safer platform for pharmaceutical research and drug development.

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