Abstract
The progressive accumulation of apoptosis-resistant and secretory active senescent cells (SCs) in animal and human aged tissues may limit lifespan and healthspan and lead to age-related diseases such as cancer, neurodegenerative disorders, and metabolic syndrome. Thus, SCs are suggested targets in anti-aging therapy. In the last two decades, a number of nanomaterials have gained much attention as innovative tools in theranostic applications due to their unique properties improving target visualization, drug and gene delivery, controlled drug release, effective diagnosis, and successful therapy. Although the healthcare industry has focused on a plethora of applications of nanomaterials, it remains elusive how nanomaterials may modulate cellular senescence, a hallmark of aging. In this review paper, we consider novel nanotechnology-based strategies for healthspan promotion and the prevention of age-related dysfunctions that are based on the delivery of therapeutic compounds capable to preferentially killing SCs (nano-senolytics) and/or modulating a proinflammatory secretome (nano-senomorphics/nano-senostatics). Recent examples of SC-targeted nanomaterials and the mechanisms underlying different aspects of the nanomaterial-mediated senolysis are presented and discussed.
Highlights
The progressive accumulation of apoptosis-resistant and secretory active senescent cells (SCs) in animal and human aged tissues may limit lifespan and healthspan and lead to age-related diseases such as cancer, neurodegenerative disorders, and metabolic syndrome
It has been revealed that diverse pathological conditions associated with accelerated aging such as cancer, neurodegenerative diseases, cardiovascular disorders, and progeroid and metabolic syndromes are accompanied by the accumulation of SCs and cellular senescence may be a causative factor for the progression of age-related pathologies [14,15,16,17,18,19]
It has been shown that panobinostat is able to increase caspase 3/7 activity and decrease the expression of anti-apoptotic proteins leading to clearance of SCs, which accumulate after anticancer drug treatment
Summary
Cellular senescence (CS) is characterized by a state of permanent cell growth arrest with altered metabolic features (e.g., affected glycolysis, mitochondrial function, and autophagic flux), modified protein secretion, and biomolecular damage that occurs in response to stressful stimuli [1,2]. The SASP entails secretion of numerous molecules, such as inflammatory chemokines (e.g., MCP-1, MIP 1α, and CCL-16) and cytokines (e.g., IL-6 and IL-8), growth factors (e.g., IGF-1 and EGF) and angiogenic factors/regulators, miRNAs, proteases, and damage-associated molecular patterns (DAMPs), which can induce changes in neighboring cells via both paracrine and autocrine mechanisms [28,29,30,31]. Apart from irreversible withdrawal from the cell cycle and SASP, another feature of SCs is their resistance to apoptosis through the multilevel regulated pro-survival senescent cell anti-apoptotic pathways (SCAPs) such as p53/p21/serpins, BCL-2/Bcl-XL , PI3K/AKT/ceramide signaling, the hypoxia-inducible factor (HIF-1α) pathway, or HSP90-dependent networks [24,30,43].
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