Hallmarks of Aging and Genomic Instability

The gradual build-up of genetic errors in the DNA within a cell over time.

A key contributor to aging, caused by the accumulation of mutations in the DNA within mitochondria, the powerhouses of our cells.

Mechanisms that help repair damaged DNA within the cell.

A protective structure that helps to maintain the shape and integrity of the nucleus of a cell. Damage to this structure can accelerate aging.

The ends of chromosomes that protect genetic information. They shorten with each cell division, contributing to aging.

Stress pathways triggered by damage to the nuclear lamina, leading to a faster aging process.

A group of genetic disorders characterized by premature aging, often caused by mutations affecting the nuclear lamina.

The ideal state where cells maintain a stable production of correctly folded proteins, without defects.

The loss of proteostasis, which occurs due to the accumulation of errors in protein production over time, is a key driver of aging and age-related diseases.

Clumps of misfolded proteins protect their interior from being broken down by cellular machinery, preventing them from being recycled.

A gene mutation that contributes to fragile protein production and a higher risk of developing Alzheimer's disease.

Metabolic processes regulated by nutrient levels, influencing aging.

A protein primarily produced by the liver in response to growth hormone, involved in glucose sensing and forming a negative feedback loop with growth hormone.

The pathway involving IGF-1 and insulin, which plays a role in glucose sensing and metabolism.

The paradox of the IIS pathway – while decreasing its activity is linked to longer lifespan, the pathway's activity actually decreases with age, potentially as a survival mechanism.

The process of DNA repair mechanisms slowing down, causing an increase in genetic errors and accelerating aging.

A process by which damaged mitochondria are removed from cells, protecting against aging and disease.

A decline in the level of NAD+ in the cell, leading to impaired communication between the nucleus and mitochondria, decreased energy production and increased ROS production.

A state where cells stop dividing and become inactive, contributing to aging and age-related diseases.

A collection of pro-inflammatory signals released by senescent cells, contributing to aging and cancer.

The ability of stem cells to differentiate into various cell types in the body, declining with age.

A decrease in the number and function of stem cells in the body, contributing to age-related decline.

Damaged mitochondria can indirectly cause mutations in their own DNA by impacting the proteins involved in their reproduction and copying process.

Apoptosis is a programmed cell death process that removes damaged cells, while senescent cells escape this process, accumulating in tissues.

The immune system becomes weaker with age, leading to the accumulation of senescent cells.

Senescent cells contribute to aging and cancer by releasing inflammatory substances that damage surrounding tissues and cells.

The pool of stem cells in our body regenerates but with lower quality and speed over time, contributing to chronic diseases.

Stem cells from early-stage embryos were initially used, but now adult cells can be reprogrammed into stem cells, called induced pluripotent stem cells (iPSCs).

The signaling chemicals that reprogram adult cells into stem cells are called Yamanaka factors, named after Nobel Prize winner Shinya Yamanaka.

Changes in cell-to-cell communication, primarily due to increased inflammation, contribute to aging and disease.

Inflammation across the body that grows with time, leading to increased activation of a chemical called NF-kB.

NF-kB is a protein complex that regulates the production of proteins, enzymes, and local signals (cytokines), playing a key role in cellular responses to stress, inflammation, and other stimuli.

The increased activity of NF-kB can cause harmful consequences as it is a master regulator of cell activity.

Cellular senescence, another hallmark of aging, is closely linked to altered intercellular communication and may be targeted for its treatment.

Aging is a complex process involving various changes, and addressing these changes may help slow down aging.

Research on aging aims to identify and modify these hallmarks to achieve healthy aging and improve overall health.