03.01
Autophagy
A cellular self-renewal process by which cells degrade and recycle damaged components. The Nobel Prize in Physiology or Medicine 2016 was awarded for autophagy research.
Mizushima, N. Autophagy: process and function. Genes & Development, 2007. Ohsumi, Y. Nobel Prize in Physiology or Medicine, 2016.
See also Mitophagy · mTOR Pathway · Spermidine
03.02
Mitophagy
A selective form of autophagy that removes damaged mitochondria. Studied in connection with mitochondrial quality control and the broader autophagy literature.
Pickles, S., Vigié, P. & Youle, R.J. Mitophagy and quality control mechanisms in mitochondrial maintenance. Current Biology, 2018.
See also Autophagy · Mitochondrial Biogenesis
03.03
Cellular Senescence
A state in which cells stop dividing while remaining metabolically active, often releasing inflammatory signals (the SASP — senescence-associated secretory phenotype). Recognized as one of the twelve hallmarks of aging.
Hayflick, L. & Moorhead, P.S. The serial cultivation of human diploid cell strains. Experimental Cell Research, 1961. Coppé, J.-P. et al. Senescence-associated secretory phenotypes reveal cell-nonautonomous functions of oncogenic RAS. PLoS Biology, 2008.
See also SASP · Fisetin · Quercetin
03.04
SASP Senescence-Associated Secretory Phenotype
The collection of cytokines, chemokines, growth factors, and proteases secreted by senescent cells. Studied in published research as a mechanism by which senescent cells influence surrounding tissue.
Coppé, J.-P. et al. The senescence-associated secretory phenotype: the dark side of tumor suppression. Annual Review of Pathology, 2010.
See also Cellular Senescence
03.05
Apoptosis
Programmed cell death — a regulated process by which cells are removed without releasing harmful contents. Distinguished from senescence (where cells persist) and necrosis (uncontrolled death).
Elmore, S. Apoptosis: A review of programmed cell death. Toxicologic Pathology, 2007.
03.06
Mitochondrial Biogenesis
The process by which new mitochondria are generated within cells. Studied as a component of mitochondrial quality control and metabolic regulation.
Ploumi, C., Daskalaki, I. & Tavernarakis, N. Mitochondrial biogenesis and clearance: a balancing act. The FEBS Journal, 2017.
See also Mitophagy · CoQ10
03.07
DNA Repair
The collection of cellular processes that identify and correct damage to DNA. Capacity for DNA repair has been studied in connection with aging biology and genomic stability.
Hoeijmakers, J.H.J. DNA damage, aging, and age-related conditions. New England Journal of Medicine, 2009.
03.08
Oxidative Stress
An imbalance between reactive oxygen species (ROS) and the body's antioxidant defenses. Studied in the context of cellular damage and aging mechanisms.
Sies, H. Oxidative stress: a concept in redox biology and medicine. Redox Biology, 2015.
See also Glutathione
03.09
Glycation AGEs — Advanced Glycation End Products
A non-enzymatic reaction between sugars and proteins or lipids that produces structurally altered molecules. AGEs have been studied in connection with tissue stiffening and aging biology.
Brownlee, M. The pathobiology of diabetic complications: a unifying mechanism. Diabetes, 2005.
03.10
Methylation
An epigenetic modification — the addition of methyl groups to DNA or proteins — that influences gene expression without altering the underlying DNA sequence. DNA methylation patterns form the basis of epigenetic clocks.
Horvath, S. DNA methylation age of human tissues and cell types. Genome Biology, 2013.
See also Epigenetic Clocks · Biological Age
03.11
Telomere Maintenance
The biological processes that preserve the protective caps at chromosome ends. Telomere length is studied in connection with cellular replicative capacity.
Blackburn, E.H., Greider, C.W. & Szostak, J.W. Nobel Prize in Physiology or Medicine, 2009. Aviv, A. & Shay, J.W. Reflections on telomere dynamics and ageing-related diseases in humans. Phil Trans R Soc B, 2018.
See also Telomere Length