Abstract

Aging in biological organisms is intricately linked to the accumulation of damage in long-lived irreparable structures, which remain unchanged throughout life. These structures include lens proteins (crystallins), DNA of postmitotic neurons, mitochondria of cardiomyocytes, tooth enamel, and centrioles of stem cells. Formed in the early stages of ontogenesis, they serve as "entropy accumulators"—a thermodynamic measure of molecular disorder. The impossibility of their replacement is dictated by evolutionary compromises: for instance, the stability of centrioles is crucial for the asymmetric division of stem cells, yet their selective inheritance results in the transfer of damage to progeny, thereby accelerating tissue aging. The accumulation of oxidized proteins, DNA mutations, and dysfunctional organelles disrupts homeostasis, triggering neurodegeneration, cataracts, and heart failure. This article examines the mechanisms underlying the damage to these structures, their role in age-related pathologies, and promising therapeutic strategies, including senolytics, CRISPR correction, and biomimetic materials. Special emphasis is placed on centrioles as key regulators of cellular entropy: while their stability supports tissue regeneration, defect accumulation leads to gene expression disruption and contributes to oncogenesis. Understanding the balance between longevity and vulnerability in irreparable structures opens new avenues for combating aging through targeted entropy management.

Keywords: aging, entropy, irreparable structures, centrioles, mitochondria, crystallins, neuronal DNA.