Selectins are involved in constitutive lymphocyte homing, and in chronic and acute inflammation processes, including post-ischemic inflammation. Each selectin has a carbohydrate recognition domain that mediates binding to specific glycans on apposing cells.

GLUT 2 is a bidirectional transporter, allowing glucose to flow in 2 directions via facilitated diffusion. Is expressed by renal tubular cells, liver cells and pancreatic beta cells. It is also present in the basolateral membrane of the small intestine epithelium.

Cellular theories of aging propose that human aging is the result of cellular aging, whereby an increasing proportion of cells reach senescence, a terminal stage at which cells will cease to divide. This will limit the body’s ability to regenerate and to respond to injury or stress. Telomeres are bits of DNA on the ends of chromosomes that protect chromosomes from sticking to each other or tangling, which could cause DNA to abnormally function. As cells replicate, telomeres shorten at the end of chromosomes, and this process correlates to senescence or cellular aging.

Other theories include:

1. The Free Radical Theory: Implicates the gradual accumulation of oxidative cellular damage as a fundamental driver of cellular aging. This theory has evolved over time to emphasize the role of free radical induced mitochondrial DNA (mtDNA) mutations and the accumulation of mtDNA deletions. Given the proximity of mtDNA to the electron transport chain, a primary producer of free radicals, it postulates that the mutations would promote mitochondrial dysfunction and concomitantly increase free radical production in a positive feedback loop. It is known that diet, lifestyle, drugs (e.g. tobacco and alcohol) and radiation etc., are all accelerators of free radical production within the body.
2. Error theory: based on the idea that errors can occur in the transcription of the synthesis of DNA. These errors are perpetuated and eventually lead to systems that do not function at the optimum level. The organism’s aging and death are attributable to these events (Sonneborn, 1979).
3. The Cross-Linking Theory: also referred to as the Glycosylation Theory of Aging. In this theory it is the binding of glucose (simple sugars) to protein, (a process that occurs under the presence of oxygen) that causes various problems. Once this binding has occurred the protein becomes impaired and is unable to perform as efficiently. Living a longer life is going to lead to the increased possibility of oxygen meeting glucose and protein and known cross-linking disorders include senile cataract and the appearance of tough, leathery and yellow skin.
4. The Neuroendocrine Theory First proposed by Professor Vladimir Dilman and Ward Dean MD, this theory elaborates on wear and tear by focusing on the neuroendocrine system. This system is a complicated network of biochemicals that govern the release of hormones which are altered by the walnut sized gland called the hypothalamus located in the brain. The hypothalamus controls various chain-reactions to instruct other organs and glands to release their hormones etc. The hypothalamus also responds to the body hormone levels as a guide to the overall hormonal activity. But as we grow older the hypothalamus loses it precision regulatory ability and the receptors which uptake individual hormones become less sensitive to them. Accordingly, as we age the secretion of many hormones declines and their effectiveness (compared unit to unit) is also reduced due to the receptors down-grading
5. The Membrane Theory of Aging: According to this theory it is the age-related changes of the cell’s ability to transfer chemicals, heat and electrical processes that impair it. As we grow older the cell membrane becomes less lipid (less watery and more solid). This impedes its efficiency to conduct normal function and in particular there is a toxic accumulation
6. The Decline Theory: The mitochondria are the power producing organelles found in every cell of every organ. Their primary job is to create Adenosine Triphosphate (ATP) and they do so in the various energy cycles that involve nutrients such as Acetyl-L-Carnitine, CoQ10 (Idebenone), NADH and some B vitamins etc. Enhancement and protection of the mitochondria is an essential part of preventing and slowing aging. Enhancement can be achieved with the above mention nutrients, as well as ATP supplements themselves.

Interphase is divided into three phases: G1 (first gap), S (synthesis), and G2 (second gap). During all three parts of interphase, the cell grows by producing proteins and cytoplasmic organelles. However, chromosomes are replicated only during the S phase. Thus, a cell grows (G1), continues to grow as it duplicates its chromosomes (S), grows more and prepares for mitosis (G2), and finally divides (M) before restarting the cycle.

Apoptosis is a programmed form of cell death involving the degradation of cellular constituents by a group of cysteine proteases called caspases. The caspases can be activated through either the intrinsic (mitochondrial mediated) or extrinsic (death receptor mediated) apoptotic pathways.

The intrinsic apoptotic pathway, also known as the mitochondrial pathway, is primarily initiated within the mitochondria. This pathway is activated in response to various internal stimuli, such as DNA damage, oxidative stress, and other cellular stresses.

When the intrinsic pathway is triggered, several events occur in the mitochondria:

1. Release of cytochrome c: Cytochrome c is released from the mitochondrial intermembrane space into the cytoplasm.
2. Formation of the apoptosome: Cytochrome c in the cytoplasm binds to apoptotic protease activating factor-1 (Apaf-1) and procaspase-9, forming a complex known as the apoptosome.
3. Activation of caspase-9: The apoptosome activates caspase-9, an initiator caspase.
4. Caspase cascade: Activated caspase-9 then activates executioner caspases, such as caspase-3, leading to the execution phase of apoptosis, which results in the orderly dismantling of the cell.

The mitochondria play a crucial role in this pathway by regulating the release of pro-apoptotic factors that are essential for the activation of downstream apoptotic processes.

Cadherins play a role in maintaining cell and tissue structure, and in cellular movement. The E-cadherin–catenin complex plays a key role in cellular adhesion; loss of this function has been associated with greater tumour metastasis.

Dynamic instability refers to the coexistence of assembly and disassembly at the ends of a microtubule. The microtubule can dynamically switch between growing and shrinking phases in this region. Although both assembly and disassembly occur at both ends they occur preferentially at the (+) end.

Carbamoyl phosphate is converted to citrulline by ornithine transcarbamoylase.

The major motor proteins that interact with microtubules are kinesin, which usually moves toward the (+) end of the microtubule, and dynein, which moves toward the (−) end.

The lysosome maintains its pH differential by pumping in protons (H+ ions) from the cytosol across the membrane via proton pumps and chloride ion channels. Vacuolar H+-ATPases are responsible for transport of protons, while the counter transport of chloride ions is performed by ClC-7 Cl−/H+ antiporter.