Abstract:
Autophagy is a natural cellular process that removes damaged organ cells and proteins. It is strongly influenced by fasting duration. Autophagy is a highly regulated cellular process that plays a crucial role in maintaining homeostasis by degrading damaged organelles and misfolded proteins. Fasting is one of the most effective methods for activating autophagy, triggering a cascade of biochemical processes at the molecular level. This article presents a mathematical framework to describe the dynamics of autophagy activation as a function of fasting duration.
Introduction
Autophagy is the body's natural process of cleaning out damaged cells and recycling them to maintain health. It helps remove waste, fight diseases, and enhance cell function. This process is crucial for longevity, immunity, and overall well-being.
Fasting has been extensively studied for its effects on metabolism, longevity, and cellular repair mechanisms. One of the most significant outcomes of fasting is the induction of autophagy, a catabolic process in which cells degrade and recycle intracellular components. This process is tightly controlled by nutrient-sensing pathways such as mTOR, AMPK, and sirtuins.
To better understand how fasting influences autophagy, we introduce mathematical models that describe the relationship between fasting duration and key biochemical markers of autophagy.
Autophagy modulation is explored as a therapeutic strategy for various diseases. Evidence suggests that intermittent fasting or calorie restriction induces adaptive autophagy, promoting cell longevity. However, excessive autophagy from prolonged restriction can trigger cell death. While calorie deprivation and autophagy are closely linked, the precise molecular mechanisms remain unclear. Here, we highlight the mathematical modeling of this process.