Aging

Aging itself can be described as the accumulation of extracellular and intracellular damage in the form of molecular aggregates, mitochondrial dysfunction, chronic inflammation, fibrosis and reduced regeneration. It can also be defined as the preclinical or presymptomatic stage of age-related diseases, such as: myocardial infarction, stroke, sarcopenia, type 2 diabetes, cataract, cancer, arthritis, Alzheimer's disease, Parkinson's The disease...Aging is also the cause of the destruction of homeostasis, leading to an increased risk of morbidity, mortality and general frailty.

Mechanism of aging

According to modern concepts, aging refers to errors accumulated at different levels of the life system: molecules, cells, tissues, organ specificity, and systemicity. However, perceptions of this cumulative cause may be different. Some authors (Gladyshev, Golubev) believe that the main reason for the accumulation of errors is the inability of the cell repair system to eliminate certain types of damage. Proponents of procedural aging (Skulachev, Mittendorf) postulate that there is an evolutionary deterministic mechanism that is induced at certain stages of ontology formation to eliminate individuals to release space and resources for the next generation. It should be noted that no genes, hormones or body structures that have evolved to establish aging have been found in humans. According to another view, aging is a quasi-procedure, which is a side effect of overactivation of compensation mechanisms that respond to the accumulation of damage and errors. Finally, the more generally accepted view is that the exponential rate of error accumulation is explained by the gradual failure of repair and maintenance systems.

The rate of accumulation of metabolic errors varies from person to person. Morbidity is partly determined by genetic susceptibility (10-25%). Some examples of genetic components of aging are: mutations in Werner and Hutchinson-Gilford Progeria, genes associated with cancer, diabetes, atherosclerosis, and dementia. However, to a greater extent, metabolic errors are related to the influence of factors in the internal and external environment: toxins, ionizing radiation, smoking, alcohol, vigorous physical activity, reactive oxygen species and nitrogen species, and activation of aging-related signaling pathways Through specific metabolites (methionine, BCAA, oxysterol, AGEs). It is worth noting that this situation involves epigenetics, because all these factors affect gene activity. In a healthy young body, instances of metabolic errors will be cleared, repaired, cleared or replaced. However, these failures in the recovery system itself will gradually accumulate with age, which will lead to the loss of dynamic balance maintenance and adaptability.

There are many signs of aging, and listing them requires some sort of classification. All components of aging, such as gene expression disorders or DNA mutations, can be divided into primary damage, response to damage, and systemic phenomena:

  • Primary damage: Genome instability, loss of protein homeostasis, epigenetic changes, respiratory system damage, non-enzymatic modification and fragmentation of extracellular matrix;
  • Inadequate response to injury: malnutrition induction, mitochondrial dysfunction, cell aging;
  • Systemic: Depletion of the stem cell pool and impaired communication between cells.

Each of these categories can be expanded to more specific topics. For example, the main damage is:

  • Genome instability: shortened telomeres, transposition of movable genetic elements, mutations and chromosomal aberrations;
  • Epigenetic changes: chromatin remodeling, changes in DNA methylation and epitope mutations, changes in histone modifications and variant histone ratios, and changes in non-coding RNA patterns;
  • Loss of protein denaturation: carbonylation aggregates, long-lived intracellular and extracellular protein cross-linking, endoplasmic reticulum stress, proteasome and autophagy inhibition, chaperone protein expression changes, and extracellular matrix fragmentation;
  • Respiratory system damage: clonal amplification and deletion of mtDNA, accumulation of oxidized guanine in mtDNA, reduction of mitochondrial gene expression, release of inflammatory formyl peptides and oxidized circular DNA in mitochondria, damage to the respiratory chain and mitochondrial enzymes, LON Reduction of protease activity.

Although these destructive processes are inherently harmful, overreaction to them is equally dangerous. As aging progresses, pressure response systems tend to become more erroneous, leading to:

  • Physiological dysfunction: neuroendocrine shift, dysregulation of intercellular signal transduction, degeneration of thymus, and suppression of adaptive immunity, at the same time, innate immune (inflammation) hyperfunction, epigenetic dysregulation of gene expression;
  • Deterioration of tissue regeneration: due to the breakdown of extracellular matrix, dysregulation of cell apoptosis, changes in stem cell wall changes (differentiation mainly depends on stem cell renewal), resulting in permanent cell cycle arrest, cytotoxic and inhibitory effects on the proliferation of matricriptins, ablating cells and The reduction in its number.
  • Systemic inflammation: activation of cGAS/STING/IFN, AGEs/RAGE and TLR/NF-kB signaling pathways, pro-inflammatory bone marrow cells, inflammatory cytokines released by these and senescent cells, imbalance of intestinal flora.

In general, primary injury and overreactive stress will produce systemic changes, including:

  • Relax the control of the internal clock;
  • Chronic stress
  • Increase the permeability of the tissue barrier;
  • Metabolic syndrome.

Understanding these mechanisms can develop biomarkers of aging that can be used to monitor individual age-dependent changes at the molecular level. Tracking human aging is achieved through the clock of aging, and the clock helps to establish new hypotheses and can be used to verify the efficacy of anti-aging therapies.

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