Our Aging Cells

Cells are the fundamental building blocks of all living organisms, providing the basic structure, extracting energy from food, following plans from genetic codes, and driving the processes required for growth, repair, and reproduction. Cells accumulate damage from DNA mutations, telomere shortening, oxidative stress, and other sources. Damage to DNA from any source that is not promptly repaired can trigger the cell's transition to a senescent state.

Although senescent cells lower cancer risk, these dysfunctional "zombie cells" accumulate with age. As dysfunctional non-dividing cells, they can no longer contribute to the specialized function of their tissues. They induce neighboring cells to become senescent and secrete toxic inflammatory signals that degrade surrounding tissues and drive age-related diseases. They stubbornly persist because, unlike most cells, they have evolved pathways that block apoptosis so they cannot commit suicide. These accumulated senescent cells are major contributors to the aging process.

As cells experience injuries the speed and effectiveness of their repair and regeneration systems strongly influence their survival. Thankfully, evolution has equipped us with powerful repair systems that routinely fix cellular damage often before it becomes irreversible. A growing body of evidence in animal studies suggests that repair systems are crucial in delaying aging, extending lifespan, and protecting against age-related diseases.

Investigators have identified fundamental biological processes known as hallmarks of aging, that drive aging and age-related diseases. Cellular senescence is considered one of the key hallmarks of aging. Therapies that remove senescent cells (senolytics) or suppress their harmful secretions (senomorphics) are being investigated as treatments for both aging itself and chronic diseases of aging. Multiple animal studies have shown that senolytics can slow the features of aging, improve physical and cognitive function