Analytics

This article concludes our series on the Hallmarks of Aging and on the ways science may be able to influence them. Earlier in the series, we introduced the topic in an overview of the rejuvenation field, and then explored specific mechanisms in articles on genetic and epigenetic changes, protein quality control, mitochondria, and cellular senescence, and autophagy, metabolism, and stem cells. Here we focus on the final three: altered intercellular communication, chronic low-grade inflammation, and dysbiosis.

We continue to explore the causes of aging in the body, known as the hallmarks of aging, and how humanity can already influence them today in an attempt to achieve rejuvenation. Earlier, we looked at the general concept of the hallmarks of aging, as well as what can already be done about aging-related causes connected with DNA damage, telomere shortening, and epigenetic alterations, and loss of protein quality control, mitochondrial dysfunction, and cellular senescence.

Aging had long appeared to be a slow wear and tear of everything at once. As we previously mentioned, it is increasingly described today as a set of specific malfunctions that can be measured and partly corrected in animal experiments. This article looks at what can already be done about aging associated with such hallmarks as protein quality control, mitochondrial function (the cell’s power plants), and the accumulation of senescent cells – those that have stopped dividing and functioning for the benefit of the organism yet continue to damage the surrounding environment. These processes reinforce one another.