Molecular Mechanisms to Target Cellular Senescence in Aging and Disease

Marcozzi, Serena; Beltrami, Antonio Paolo; Malavolta, Marco

doi:10.3390/cells11233732

Cited by 6 publications

(3 citation statements)

References 21 publications

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“…Cellular senescence is characterized by high heterogenicity and the expression of complex phenotypes [ 2 , 7 ]. Many cellular and molecular signatures have been exploited as senescent markers, however, none of them are exclusively expressed in senescent cells [ 4 ]. In view of this, the combination usage of biomarkers emerges as an effective way to achieve specific and accurate recognition of senescent cells.…”

Section: Dual-targeting Fluorescent Sensors For Precisely Tracking Ce...mentioning

confidence: 99%

“…Cellular senescence, an irreversible state of cell cycle arrest, was firstly described in the 1960s by Hayflick and colleagues [ 1 , 2 ]. In addition to replicative senescence in which the shortening of telomeres is involved, senescence has been revealed to be related to various cellular stresses, such as DNA damage and reactive oxygen species (ROS), and thus is closely associated with a broad range of biological processes and diseases [ 3 , 4 , 5 ]. With increasing knowledge on the positive and negative aspects of cellular senescence, senescent cells have been recognized as attractive targets for antiaging approaches.…”

Section: Introductionmentioning

confidence: 99%

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Molecularly Targeted Fluorescent Sensors for Visualizing and Tracking Cellular Senescence

He,

Xu,

et al. 2023

Biosensors

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Specific identification and monitoring of senescent cells are essential for the in-depth understanding and regulation of senescence-related life processes and diseases. Fluorescent sensors providing real-time and in situ information with spatiotemporal resolution are unparalleled tools and have contributed greatly to this field. This review focuses on the recent progress in fluorescent sensors for molecularly targeted imaging and real-time tracking of cellular senescence. The molecular design, sensing mechanisms, and biological activities of the sensors are discussed. The sensors are categorized by the types of markers and targeting ligands. Accordingly, their molecular recognition and fluorescent performance towards senescence biomarkers are summarized. Finally, the perspective and challenges in this field are discussed, which are expected to assist future design of next-generation sensors for monitoring cellular senescence.

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Section: Dual-targeting Fluorescent Sensors For Precisely Tracking Ce...mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Molecularly Targeted Fluorescent Sensors for Visualizing and Tracking Cellular Senescence

He,

Xu,

et al. 2023

Biosensors

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“…Given that triggering cancer cell dormancy following conventional cancer therapies is almost inevitable, some authors have suggested a 'one-two punch' strategy in which the sequential treatment of cancer with pro-senescence therapy is followed by "senolytic" therapy [68,69]. Time will tell whether such an approach can be used to significantly improve the length and quality of life of cancer patients.…”

Section: Introductionmentioning

confidence: 99%

When Therapy-Induced Cancer Cell Apoptosis Fuels Tumor Relapse

Mirzayans

2024

Onco

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Most therapeutic strategies for solid tumor malignancies are designed based on the hypothesis that cancer cells evade apoptosis to exhibit therapy resistance. This is somewhat surprising given that clinical studies published since the 1990s have demonstrated that increased apoptosis in solid tumors is associated with cancer aggressiveness and poor clinical outcome. This is consistent with more recent reports demonstrating non-canonical (pro-survival) roles for apoptotic caspases, including caspase 3, as well as the ability of cancer cells to recover from late stages of apoptosis via a process called anastasis. These activities are essential for the normal development and maintenance of a healthy organism, but they also enable malignant cells (including cancer stem cells) to resist anticancer treatment and potentially contribute to clinical dormancy (minimal residual disease). Like apoptosis, therapy-induced cancer cell dormancy (durable proliferation arrest reflecting various manifestations of genome chaos) is also not obligatorily a permanent cell fate. However, as briefly discussed herein, compelling pre-clinical studies suggest that (reversible) dormancy might be the “lesser evil” compared to treacherous apoptosis.

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