Cellular senescence in the context of "Beta-galactosidase"

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⭐ Core Definition: Cellular senescence

Cellular senescence is a phenomenon characterized by the cessation of cell division. In their experiments during the early 1960s, Leonard Hayflick and Paul Moorhead found that normal human fetal fibroblasts in culture reach a maximum of approximately 50 cell population doublings before becoming senescent. This process called the Hayflick limit is also known as "replicative senescence", since it is brought about through replication. Hayflick's discovery of mortal cells paved the path for the discovery and understanding of cellular aging molecular pathways. Cellular senescence can be initiated by a wide variety of stress-inducing factors. These stress factors include both environmental and internal damaging events, abnormal cellular growth, oxidative stress, autophagy factors, among many other things.

The physiological importance of cell senescence has been attributed to prevention of carcinogenesis, and more recently, aging, development, and tissue repair. Senescent cells contribute to the aging phenotype, including frailty syndrome, sarcopenia, and aging-associated diseases. Senescent astrocytes and microglia contribute to neurodegeneration.

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Cellular senescence in the context of Ageing

Ageing (or aging in American English) is the process of becoming older. The term refers mainly to humans, many other animals, and fungi; whereas for example, bacteria, perennial plants and some simple animals are potentially biologically immortal. In a broader sense, ageing can refer to single cells within an organism which have ceased dividing, or to the population of a species.

In humans, ageing represents the accumulation of changes in a human being over time and can encompass physical, psychological, and social changes. Reaction time, for example, may slow with age, while memories and general knowledge typically increase. Of the roughly 150,000 people who die each day across the globe, about two-thirds die from age-related causes.

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Cellular senescence in the context of Hayflick limit

The Hayflick limit, or Hayflick phenomenon, is the number of times a normal somatic, differentiated human cell population will divide before cell division stops.

The concept of the Hayflick limit was advanced by American anatomist Leonard Hayflick in 1961, at the Wistar Institute in Philadelphia, Pennsylvania. Hayflick demonstrated that a normal human fetal cell population will divide between 40 and 60 times in cell culture before entering a senescence phase. This finding refuted the contention by Alexis Carrel that normal cells are immortal.

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Cellular senescence in the context of Phagosome

In cell biology, a phagosome is a vesicle formed around a particle engulfed by a phagocyte via phagocytosis. Professional phagocytes include macrophages, neutrophils, and dendritic cells (DCs).

A phagosome is formed by the fusion of the cell membrane around a microorganism, a senescent cell or an apoptotic cell. Phagosomes have membrane-bound proteins to recruit and fuse with lysosomes to form mature phagolysosomes. The lysosomes contain hydrolytic enzymes and reactive oxygen species (ROS) which kill and digest the pathogens. Phagosomes can also form in non-professional phagocytes, but they can only engulf a smaller range of particles, and do not contain ROS. The useful materials (e.g. amino acids) from the digested particles are moved into the cytosol, and waste is removed by exocytosis. Phagosome formation is crucial for tissue homeostasis and both innate and adaptive host defense against pathogens.

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Cellular senescence in the context of Lipopolysaccharide

Lipopolysaccharide (LPS), now more commonly known as endotoxin, is a collective term for components of the outermost membrane of the cell envelope of gram-negative bacteria, such as E. coli and Salmonella with a common structural architecture. Lipopolysaccharides are large molecules consisting of three parts: an outer core polysaccharide termed the O-antigen, an inner core oligosaccharide and Lipid A (from which toxicity is largely derived), all covalently linked. In current terminology, the term endotoxin is often used synonymously with LPS, although there are a few endotoxins (in the original sense of toxins that are inside the bacterial cell that are released when the cell disintegrates) that are not related to LPS, such as the so-called delta endotoxin proteins produced by Bacillus thuringiensis.

Lipopolysaccharides can have substantial impacts on human health, primarily through interactions with the immune system. LPS is a potent activator of the immune system and is a pyrogen (agent that causes fever). In severe cases, LPS can trigger a brisk host response and multiple types of acute organ failure which can lead to septic shock. In lower levels and over a longer time period, there is evidence LPS may play an important and harmful role in autoimmunity, obesity, depression, and cellular senescence.

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Cellular senescence in the context of Karyorrhexis

Karyorrhexis (from Greek κάρυον karyon, "kernel, seed, nucleus," and ῥῆξις rhexis, "bursting") is the destructive fragmentation of the cell nucleus that occurs in a dying cell. It is characterized by the breakdown of the nuclear envelope and the dispersal of condensed chromatin into the cytoplasm. The process is usually preceded by pyknosis (irreversible chromatin condensation) and followed by karyolysis (enzymatic dissolution of chromatin). It may occur during programmed cell death (apoptosis), cellular senescence, or necrosis.

In apoptosis, karyorrhexis is mediated by Ca- and Mg-dependent endonucleases, ensuring that nuclear fragments are packaged into apoptotic bodies and removed by phagocytosis. In necrosis, by contrast, nuclear fragmentation occurs in a less orderly fashion, leaving behind cellular debris that can contribute to tissue damage and inflammation.

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