Aging is a complex biological process that leads to the gradual decline in cellular and physiological functions, ultimately increasing the risk of age-related diseases. In the Kumsta Lab, our research focuses on deciphering the molecular mechanisms that contribute to aging, with particular emphasis on proteostasis, autophagy, and inter-tissue communication.
Proteostasis, or protein homeostasis, refers to the delicate balance of protein synthesis, folding, and degradation within cells. As we age, this balance becomes disrupted, leading to the accumulation of misfolded or damaged proteins, which can contribute to cellular dysfunction and the onset of age-related diseases. An integral aspect of proteostasis is the cellular stress response, a protective mechanism activated in response to various stressors such as, heat shock, oxidative damage, and toxins. Stress responses help to maintain proteostasis by upregulating the expression of molecular chaperones, autophagy genes and proteasomes, and other components involved in protein quality control. Our lab investigates these stress responses and their role in preserving proteostasis, aiming to identify strategies to bolster these protective mechanisms in aging cells.
Hormesis is a biological phenomenon where exposure to low levels of stress or toxins can actually enhance cellular function and promote longevity. This paradoxical response involves the activation of protective mechanisms, such as stress responses and autophagy, which help the organism to cope with and adapt to mild stress. In the context of aging, hormesis plays a critical role in maintaining cellular homeostasis and preventing age-related decline. Our lab explores how controlled exposure to mild stressors can trigger hormetic responses, potentially offering novel strategies to delay aging and improve healthspan. By understanding the molecular pathways underlying hormesis, we aim to harness these responses to bolster cellular resilience and promote healthy aging.
Autophagy is a cellular process responsible for the degradation and recycling of damaged cellular components, including proteins and organelles. This self-cleaning mechanism is crucial for cellular health and longevity. However, autophagy declines with age, leading to the accumulation of cellular debris and contributing to the progression of age-related disorders. Our research aims to understand the regulation of autophagy in aging and how enhancing this process can improve cellular function and delay the onset of age-related diseases.
Inter-tissue communication refers to the complex signaling networks that allow different tissues and organs to coordinate their functions. As organisms age, these communication pathways can become impaired, leading to systemic imbalances that contribute to aging and disease. Our lab is dedicated to uncovering the molecular signals that govern inter-tissue communication, with the goal of identifying how these pathways can be modulated to promote healthy aging across the entire organism.