There are some human single cell aging data,
Currently, ``biological aging'' is well defined in human beings and multicellular organisms, and is one of the largest risk factors for most diseases. However, in single cell organisms there has been a sequence of various definitions. My research focuses on understanding the cellular processes responsible for senescence and death in E. coli bacteria as well as identifying cellular characteristics of aging. We employed an experimental setup consisting of a microfluidic device designed to trap single-cells while continuously supplying them with nutrients, allowing us to acquire images of the trapped cells. Analysis of these images provides long-term single-cell measurements of cell-size and protein content, which are then used to uncover aging effects and determine modes of cell death. Our data acquired thus far reveal two different phenotypes of cell death: 1. Part of the cells maintain their bacterial chromosome and enter a non-dividing phase. 2. A subset of the population loses its chromosome and so all cellular functions are obstructed. Our results indicate aging in all strains, which is marked by the increase in death rate with time. In addition, by comparing wild type and an ATP synthase E. coli mutant, we found different average lifetimes prior to undergoing these transitions.
https://www.sciencefocus.com/the-human-body/what-cells-in-the-human-body-live-the-longest/#:~:text=Although%20the%20our%20bodies%20are,around%20for%20longer%20than%20others.&text=On%20average%2C%20the%20cells%20in,different%20organs%20of%20the%20body.
on average: 7-10
neutrophils, white cell: 2 days
cell in the middle eye lenses: entire lifespan of the host
brain cells: might live longer than the host
Brain cells: 200+ years?
Eye lens cells: Lifetime
Egg cells: 50 years
Heart muscle cells: 40 years
Intestinal cells (excluding lining): 15.9 years
Skeletal muscle cells: 15.1 years
Fat cells: 8 years
Hematopoietic stem cells: 5 years
Liver cells: 10-16 months
Pancreas cells: 1 year
Santra, Deill, and de Graff, PNAS 2019
use folded and unfoled protein, damage to model aging.
Imai and Kitano 1998 heterochromatin islands hypothesis for cellular aging
https://pubmed.ncbi.nlm.nih.gov/9789733/
The mechanism of cellular aging has been suggested to play an important role in organismic aging, but the molecular linkage between them is not still understood. The recent progress in the studies of telomere and telomerase demonstrates their substantial roles in the mechanism of cellular aging. On the other hand, these studies also raise controversial issues about the generality of the telomere hypothesis. The heterochronic, polymorphic, and probabilistic features of cellular aging should be reconsidered critically. In this review, we attempt to develop a general scheme for the driving force of cellular aging, based on our molecular and computational studies. Our molecular analyses suggest that global transcriptional repressive structures are essentially involved in cellular aging-associated transcriptional regulation. From our theoretical studies, systematic reorganization of these repressive structures are suggested to be a fundamental driving force of cellular aging. The heterochromatin island hypothesis is proposed to give a rational explanation for the three distinctive features of cellular aging. The importance of a dynamic equilibrium in heterochromatin islands is also discussed for cellular and organismic aging.
https://pubmed.ncbi.nlm.nih.gov/9315443/
There are significant changes in gene expression that occur with cellular senescence and organismic aging. Genes residing in compacted heterochromatin domains are typically silenced due to an altered accessibility to transcription factors. Heterochromatin domains and gene silencing are set up in early development and were initially believed to be maintained for the remainder of the lifespan. Recent data suggest that there may be a net loss of heterochromatin with advancing age in both yeast and mice. The gradual loss of heterochromatin-induced gene silencing could explain the changes in gene expression that are closely linked with aging. A general model is proposed for heterochromatin loss as a major factor in generating alterations in gene expression with age. The heterochromatin loss model is supported by several lines of evidence and suggests that a fundamental genetic mechanism underlies most of the changes in gene expression observed with senescence.
