Controlling 'Zombie Cells' in the Body to Prevent Aging

Seoul National University Professor Kang Chanhee's Team Presents New Possibilities for Aging Treatment

Reference photo. [Image source=Yonhap News]

[Asia Economy Reporter Kim Bong-su] Domestic researchers have uncovered the core mechanism of aging, bringing humanity one step closer to the long-standing aspiration of 'disease-free longevity.'

Seoul National University announced on the 29th that Professor Kang Chan-hee's research team from the Department of Life Sciences identified a new regulatory mechanism that maintains the characteristics of senescent cells, presenting new possibilities for aging treatment through the control of senescent cells.

In 2018, the World Health Organization (WHO) officially included aging in the International Classification of Diseases (Code MG2A: Old age), accelerating research to overcome aging. At the forefront of this research is the removal of senescent cells, often called 'zombie cells' in the body. 'Cellular senescence' refers to the phenomenon where normal cells permanently stop dividing due to various stresses. When young, the immune system removes senescent cells to maintain bodily homeostasis. However, as one ages, senescent cells that escape immune surveillance accumulate, causing various aging-related diseases such as cancer, cardiovascular diseases, and degenerative disorders.

Recently, research showing that the removal of senescent cells, known as 'senolysis,' can significantly improve aging and aging-related diseases has attracted global attention. However, senescent cells are highly resistant to various stresses compared to normal cells, making them difficult to eliminate. They secrete various factors called the 'senescence-associated secretory phenotype' (SASP), which can transform surrounding normal cells into senescent or cancerous cells, much like 'zombies' in movies, making treatment practically impossible.

To elucidate the 'stress support network' that maintains these characteristics of senescent cells, the research team focused on factors whose stability specifically changes during the cellular senescence response. To this end, they newly developed a 'selective autophagy target discovery platform' and identified numerous factors whose stability significantly decreases due to autophagy (the cell's 'core degradation factory') during the cellular senescence response.

Further research revealed that the degradation of these newly identified factors greatly increases the resistance of senescent cells to oxidative stress and protein toxicity, and also significantly promotes the secretion of various inflammation-inducing factors that harm surrounding cells.

Moreover, when the selective degradation of each factor was artificially inhibited, senescent cells lost their characteristic zombie-like activity and exhibited responses similar to normal cells. The team also discovered that this regulation occurs in tissues of patients with degenerative arthritis, a representative aging-related disease.

Professor Kang Chan-hee stated, "This research is significant in demonstrating that the activity of senescent cells, a major cause of aging, can be controlled through selective autophagy regulation. We will strive to establish effective senolysis strategies using this approach." He added, "The selective autophagy target platform can also be utilized to find regulatory mechanisms of cancer cell characteristics."

The research findings were published on the 29th in 'Developmental Cell,' a sister journal of Cell, the most prestigious journal in the life sciences field.

This content was produced with the assistance of AI translation services.