Aging may be a program, not a breakdown
Recorded: Sept. 22, 2026, 5 p.m.
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Why Aging May Be a Program, Not a Breakdown | Quanta Magazine
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Comment Comments Save Article Read Later Q&A By Ingrid Wickelgren August 14, 2026 By deciphering the molecular signatures of millions of mouse cells, Junyue Cao has found that aging is not haphazard wear and tear but rather a “remodeling of the cell society.” Comment Save Article Read Later
Junyue Cao, a cell biologist at Rockefeller University in New York City, analyzed gene expression in millions of mouse cells from different life stages. He was surprised to find that “changes in aging are not universal across all the cells,” he said. Karen Dias for Quanta Magazine Introduction
By Ingrid Wickelgren August 14, 2026 View PDF/Print Mode aging animals biology cell biology cells developmental biology epigenetics gene expression genomics proteins Q&A All topics In some ways, we know aging when we see it, from the graying of hair to the wrinkling of skin to declines in motor, sensory, and cognitive capacities. Yet the underlying biology of aging remains a matter of uncertainty and debate. Many lines of research align with the theory that aging is a direct result of decay — the inevitable degradation of molecules (including proteins or DNA), organelles, cells, or whole organs — from external assault or inexorable breakdown. When the body’s repair mechanisms fail to keep pace with these changes, like a factory with deteriorating equipment and too few mechanics, it manifests as the known signs of aging and, eventually, death. Share this article Copied! Copy link Ycombinator
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In graduate school, Cao developed tools to identify changes in gene expression during embryonic development in mice. Now his lab applies these tools across an animal’s entire lifespan. Karen Dias for Quanta Magazine In one series of experiments, Cao and his team processed 21 million cells, sampled from 14 tissues or organs in about 50 male and female mice at five life stages, and built a data set of gene expression for each cell. “It’s extremely large-scale data,” Cao said. “You know which organ it’s from and which age it’s from, and you also know extensive molecular information.” Each stage was marked by a dramatic decline in or expansion of specific cell types.
Cao’s analysis required enormous volumes of data: tens of thousands of gene expression changes across 21 million cells, sampled from 14 tissues or organs in about 50 male and female mice at five life stages. Karen Dias for Quanta Magazine After I graduated, I moved to the U.S. and worked at the Jackson Laboratory [a Maine-based biomedical research nonprofit] as a research assistant studying molecular pathways associated with aging in mice. I thought that by studying pathways, we could identify a [drug] target and, from there, develop drugs to increase lifespan.
During distinct time windows as an animal ages, different cell types undergo distinct dynamics, according to Cao’s lab’s experiments. Some expand, some decline, and others remain stable. Karen Dias for Quanta Magazine Can you describe those experiments and what you learned from them?
“Our claim is that aging is not so much molecular damage as a remodeling of the entire cell society,” Cao said. Karen Dias for Quanta Magazine Between 6 and 12 months in a mouse [equivalent to a person in their 30s and 40s], we see dramatic depletion of cells needed to maintain the body’s tissues. These include tenocytes [the primary component of tendons]; the cells that wrap around blood vessels and stabilize the circulatory system; the smooth muscle cells of the colon; and kidney epithelial cells, which filter toxins from the blood. Also in decline are some immune cells that protect specific tissues such as the intestine.
Cao’s research suggests that in humans the aging program begins before age 30. Karen Dias for Quanta Magazine What controls this cellular remodeling in aging, if anything? Related: Why Do We Get Old, and Can Aging Be Reversed? Epigenetic ‘Clocks’ Predict Animals’ True Biological Age Cells Across the Body Talk to Each Other About Aging What type of signaling?
By Ingrid Wickelgren August 14, 2026 View PDF/Print Mode aging animals biology cell biology cells developmental biology epigenetics gene expression genomics proteins Q&A All topics Share this article Copied! Copy link Ycombinator
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The concept of aging is increasingly viewed not as a haphazard breakdown resulting from the linear accumulation of molecular damage, such as degradation of proteins or DNA, but rather as a programmed, stepwise process that involves the remodeling of the entire cell society. This perspective, developed through the analysis of molecular signatures in mouse cells, suggests that aging follows distinct developmental stages, similar to embryonic development rather than a simple progression of decay. Research conducted by Junyue Cao and colleagues involved analyzing gene expression across millions of mouse cells sampled from various tissues and organs at multiple life stages. This extensive, high-throughput data revealed that the changes associated with aging are not universal across all cell types; instead, they manifest as coordinated dynamics involving specific populations of cells. This approach posits that aging is fundamentally a reorganization of the body's cellular architecture rather than solely a degradation of individual components. The study delineated several distinct windows during which cellular dynamics shift. In the early phase of aging, observed in young mice, there is a depletion of certain cell types, including some fat and muscle cells, and immature cell populations within the brain that possess regenerative potential. As the process advances, between approximately six and twelve months, a dramatic depletion of cells critical for maintaining bodily tissues occurs, affecting components such as tenocytes in tendons, cells stabilizing the circulatory system, smooth muscle cells of the colon, and kidney epithelial cells, alongside certain protective immune cells. A subsequent phase involves cellular expansion, beginning around twelve months, where immune cells and cells in organs like the lungs and kidneys expand due to stress or inflammation. Later stages, around sixteen months, involve the proliferation of specialized, aging-associated immune cells, which are implied to contribute to the eventual systemic decline. These changes suggest that the system undergoes coordinated shifts across different organs and cell types as it ages. These observed cellular dynamics are consistent with the idea that aging is driven by upstream signals, which can be both internal molecular programs, such as proteins regulating gene expression, and external, secreted molecules like cytokines. The findings indicate that the body possesses a program for aging, and these abrupt changes in mammalian aging suggest that signals drive transitions between these programmed stages. Furthermore, research indicates that this remodeling process likely commences before the age of thirty in humans. The implication of viewing aging as a remodeling of the cell society is that interventions should be initiated early, as the regenerative capacity and robustness of the system demonstrably decrease prior to middle age. Identifying the specific, often vulnerable, cell types and the molecular code that orchestrates this aging program provides potential targets for anti-aging strategies aimed at reprogramming these cellular dynamics. |