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Review
. 2024 Apr 1;15(2):612-639.
doi: 10.14336/AD.2023.0621.

Underlying Mechanisms and Treatment of Cellular Senescence-Induced Biological Barrier Interruption and Related Diseases

Ruize Sun  1 , Juan Feng  1 , Jue Wang  1
Affiliations
Review

Underlying Mechanisms and Treatment of Cellular Senescence-Induced Biological Barrier Interruption and Related Diseases

Ruize Sun et al. Aging Dis. .

Abstract

Given its increasing prevalence, aging is of great concern to researchers worldwide. Cellular senescence is a physiological or pathological cellular state caused by aging and a prominent risk factor for the interruption of the integrity and functionality of human biological barriers. Health barriers play an important role in maintaining microenvironmental homeostasis within the body. The senescence of barrier cells leads to barrier dysfunction and age-related diseases. Cellular senescence has been reported to be a key target for the prevention of age-related barrier diseases, including Alzheimer's disease, Parkinson's disease, age-related macular degeneration, diabetic retinopathy, and preeclampsia. Drugs such as metformin, dasatinib, quercetin, BCL-2 inhibitors, and rapamycin have been shown to intervene in cellular senescence and age-related diseases. In this review, we conclude that cellular senescence is involved in age-related biological barrier impairment. We further outline the cellular pathways and mechanisms underlying barrier impairment caused by cellular senescence and describe age-related barrier diseases associated with senescent cells. Finally, we summarize the currently used anti-senescence pharmacological interventions and discuss their therapeutic potential for preventing age-related barrier diseases.

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Figures

Figure 1.
Figure 1.
Cellular changes and regulation of the biological barrier from youth to senescence. (A) Changes in astrocytes, pericytes, endothelial cells, microglia, neurons, and secretory factors from young BBB to senescent BBB. (B) Changes in retinal stem cells, Müller cell, RPE, pericyte, endothelium, neuron and microglial, etc., and secretory agents from young BRB to senescent BRB. (C) Changes in the peritubular cell, Sertoli cell, preleptotene spermatocyte, spermatogonium, pericyte cell, etc., and secretory elements from young BTB to senescent BTB. (D) Changes in cytotrophoblast, syncytiotrophoblast, MPC, etc., and secretory factors from young PB to senescent PB. (E) Changes in the epithelial cell, stem cell, paneth cell, and some other structure or secretory components from young IB to senescent IB.
Figure 2.
Figure 2.
Factors involved in regulating age-dependent physiological barrier diseases and their pathological processes.
See this image and copyright information in PMC

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