Abstract
Telomeres are localized at the end of chromosomes to provide genome stability; however, the telomere length tends to be shortened with each cell division inducing a progressive telomere shortening (TS). In addition to age, other factors, such as exposure to pollutants, diet, stress, and disruptions in the shelterin protein complex or genes associated with telomerase induce TS. This phenomenon favors cellular senescence and genotoxic stress, which increases the risk of the development and progression of lung diseases such as idiopathic pulmonary fibrosis, chronic obstructive pulmonary disease, SARS-CoV-2 infection, and lung cancer. In an infectious environment, immune cells that exhibit TS are associated with severe lymphopenia and death, whereas in a noninfectious context, naïve T cells that exhibit TS are related to cancer progression and enhanced inflammatory processes. In this review, we discuss how TS modifies the function of the immune system cells, making them inefficient in maintaining homeostasis in the lung. Finally, we discuss the advances in drug and gene therapy for lung diseases where TS could be used as a target for future treatments.
Highlights
Telomeres are repetitive regions of noncoding DNA localized at the end of eukaryotic chromosomes to provide genome stability
It has been reported that the telomerase, an enzyme multi-unit complex, has a catalytic component that is silent in normal cells, while it is reactivated in cancer cells to maintain telomere shortening (TS) and contributes to their indefinite proliferation to maintain tumor growth [5]
During aging has been described diverse immunological alterations that alter the balance of immune cells as the accumulation of differentiated and less proliferative T cells; in this regard, cellular senescence is characterized by the development of time-dependent changes in global gene expression, epigenetic profile, and metabolism that end when a cell shows irreversible cell cycle arrest [14]
Summary
Telomeres are repetitive regions of noncoding DNA localized at the end of eukaryotic chromosomes to provide genome stability. Other factors, such as exposure to inhalable particulate matter (PM 2.5 and 10), stress, smoking, obesity, sedentary lifestyle, poor diet, oxidative stress, DNA damage (caused by free radicals), and alterations in the shelterin complex or telomerase-associated genes promote continuous damage to cellular DNA to induce TS [10,11,12,13]. It is unclear how TS affects specific functions of immune system cells. We discuss the relationship between TS and alterations in the function of cells of the immune system as well as current advances in the development of drug and gene therapy as targets for future treatments of lung diseases
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