Building Bridges Between DNA Damage Response and GATA4 Signaling in Aging

Published on September 13, 2022

Imagine aging as a marvelous bridge, gracefully connecting the passage of time with the wear and tear on our bodies. At its core lies cellular senescence, a process that triggers when our precious DNA sustains damage. Picture this: the DNA damage response (DDR) acts as the vigilant bridgekeeper, setting off alarm bells by activating two key kinases – ATM and ATR. Fulfilling its duties, guardian p53 jumps into action, halting the cell cycle and ushering in cellular senescence. Enter GATA4, a transcription factor that normally orchestrates the development of several organs. But here’s where it gets intriguing – GATA4 also gets involved in DDR, which in turn influences aging itself. In fact, research links the GATA4 signaling pathway to various age-related diseases like atherosclerosis and heart failure. The review paper explores the intertwined relationship between GATA4, DDR, cellular senescence, and their potential impact on aging-related ailments.

Aging is the continuous degradation of biological function and structure with time, and cellular senescence lies at its core. DNA damage response (DDR) can activate Ataxia telangiectasia-mutated serine/threonine kinase (ATM) and Rad3-related serine/threonine kinase (ATR), after which p53 activates p21, stopping the cell cycle and inducing cell senescence. GATA4 is a transcription factor that plays an important role in the development of many organs, such as the heart, testis, ovary, foregut, liver, and ventral pancreas. Studies have shown that GATA4 can also contribute to the DDR, leading to aging. Consistently, there is also evidence that the GATA4 signaling pathway is associated with aging-related diseases, including atherosclerosis and heart failure. This paper reviews the relationship between GATA4, DDR, and cellular senescence, as well as its effect on aging-related diseases.

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