Here is a detailed article about the University of Tokyo’s research, presented in a polite tone and in English, based on the provided link.
University of Tokyo Researchers Uncover Key Mechanism Shielding Senescent Cells from Iron-Induced Death
Tokyo, Japan – July 30, 2025 – Researchers at the University of Tokyo have made a significant breakthrough in understanding cellular aging, identifying a crucial mechanism that prevents senescent cells from succumbing to iron-induced cell death. This discovery, published on July 29, 2025, at 09:00 JST, sheds new light on the complex processes involved in cellular senescence and could pave the way for novel therapeutic strategies.
Cellular senescence is a state where cells cease to divide and proliferate, often as a protective response to cellular damage or stress. While this process plays vital roles in tissue repair and preventing cancer, the accumulation of senescent cells over time has been increasingly linked to age-related diseases and tissue dysfunction.
One of the critical challenges in understanding senescent cells has been their unique metabolic profile and susceptibility to various forms of cellular stress. Previous research has indicated that senescent cells can accumulate iron, a metal that, under certain conditions, can trigger cell death through mechanisms like ferroptosis. However, it remained unclear how senescent cells managed to survive despite this potential vulnerability.
The team at the University of Tokyo has now elucidated a key protective mechanism. Their findings reveal that senescent cells exhibit significantly elevated levels of a specific protein, CD73 (also known as ecto-5′-nucleotidase). This enzyme plays a crucial role in purine metabolism, converting AMP (adenosine monophosphate) into adenosine.
The research demonstrates that the increased abundance of CD73 in senescent cells leads to higher levels of adenosine. Adenosine, in turn, acts as a potent anti-inflammatory and cytoprotective molecule. Importantly, the study found that adenosine effectively suppresses the activity of GPX4 (glutathione peroxidase 4), a key enzyme responsible for mitigating lipid peroxidation, the process that drives ferroptosis. By downregulating GPX4 activity, senescent cells appear to create a cellular environment that is resistant to iron-induced cell death, even in the presence of elevated iron levels.
This intricate metabolic regulation allows senescent cells to persist, a characteristic that, while potentially contributing to aging-related pathologies, is a testament to their unique survival strategies. Understanding this mechanism is critical because it offers a potential therapeutic target. If the elevated CD73 activity or the subsequent suppression of GPX4 could be modulated, it might offer a means to selectively eliminate senescent cells, a concept known as “senolysis,” without harming healthy cells.
The implications of this research are far-reaching. Senolytic therapies hold promise for treating a wide array of age-related conditions, including osteoarthritis, fibrosis, cardiovascular diseases, and neurodegenerative disorders. By understanding how senescent cells evade death mechanisms, scientists can develop more precise and effective ways to target them.
This groundbreaking work by the University of Tokyo researchers represents a significant step forward in our comprehension of cellular aging. It not only answers a fundamental question about the survival of senescent cells but also opens up new avenues for developing innovative treatments to combat the debilitating effects of aging. Further research will undoubtedly explore how to best harness this knowledge for the benefit of human health.
AI has delivered the news.
The answer to the following question is obtained from Google Gemini.
東京大学 published ‘老化した細胞が鉄で死なない仕組みを解明’ at 2025-07-29 09:00. Please write a detailed article about this news in a polite tone with relevant information. Please reply in English with the article only.