Cellular senescence in development, regeneration and disease

Rhinn, Muriel; Ritschka, Birgit; Keyes, William M.

doi:10.1242/dev.151837

Cited by 210 publications

(228 citation statements)

References 124 publications

(166 reference statements)

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“…It appears to be beneficial if intermittent, but it causes pathology if chronically active. Strategies using senolytic compounds are now issues of active research to enhance endogenous regeneration capacity [109,[125][126][127].…”

Section: Principles Of Bone Formation Maintenance and Regenerationmentioning

confidence: 99%

Interactions between Muscle and Bone—Where Physics Meets Biology

et al. 2020

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Muscle and bone interact via physical forces and secreted osteokines and myokines. Physical forces are generated through gravity, locomotion, exercise, and external devices. Cells sense mechanical strain via adhesion molecules and translate it into biochemical responses, modulating the basic mechanisms of cellular biology such as lineage commitment, tissue formation, and maturation. This may result in the initiation of bone formation, muscle hypertrophy, and the enhanced production of extracellular matrix constituents, adhesion molecules, and cytoskeletal elements. Bone and muscle mass, resistance to strain, and the stiffness of matrix, cells, and tissues are enhanced, influencing fracture resistance and muscle power. This propagates a dynamic and continuous reciprocity of physicochemical interaction. Secreted growth and differentiation factors are important effectors of mutual interaction. The acute effects of exercise induce the secretion of exosomes with cargo molecules that are capable of mediating the endocrine effects between muscle, bone, and the organism. Long-term changes induce adaptations of the respective tissue secretome that maintain adequate homeostatic conditions. Lessons from unloading, microgravity, and disuse teach us that gratuitous tissue is removed or reorganized while immobility and inflammation trigger muscle and bone marrow fatty infiltration and propagate degenerative diseases such as sarcopenia and osteoporosis. Ongoing research will certainly find new therapeutic targets for prevention and treatment.

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Section: Principles Of Bone Formation Maintenance and Regenerationmentioning

confidence: 99%

Interactions between Muscle and Bone—Where Physics Meets Biology

et al. 2020

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“…As Seen from the results in this study, we know the molecular mechanism between both manners of shoot regeneration all involved in stress-responsive programme. Senescence had a close regulatory roles regeneration [46]. Rapp et al reviewed many attributes common to senescence and dedifferentiation, so the differentiation ability was hugely affected by the senescence programme [44].…”

Section: Discussionmentioning

confidence: 99%

Identification of Shoot Differentiation-Related Genes in Populus euphratica Oliv.

Dong

Li-zhi

et al. 2019

Genes

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De novo shoot regeneration is one of the important manifestations of cell totipotency in organogenesis, which reflects a survival strategy organism evolved when facing natural selection. Compared with tissue regeneration, and somatic embryogenesis, de novo shoot regeneration denotes a shoot regeneration process directly from detatched or injured tissues of plant. Studies on plant shoot regeneration had identified key genes mediating shoot regeneration. However, knowledge was derived from Arabidopsis; the regeneration capacity is hugely distinct among species. To achieve a comprehensive understanding of the shoot regeneration mechanism from tree species, we select four genetic lines of Populus euphratica from a natural population to be sequenced at transcriptome level. On the basis of the large difference of differentiation capacity, between the highly differentiated (HD) and low differentiated (LD) groups, the analysis of differential expression identified 4920 differentially expressed genes (DEGs), which were revealed in five groups of expression patterns by clustering analysis. Enrichment showed crucial pathways involved in regulation of regeneration difference, including "plant hormone signal transduction", "cell differentiation", "cellular response to auxin stimulus", and "auxin-activated signaling pathway". The expression of nine genes reported to be associated with shoot regeneration was validated using quantitative real-time PCR (qRT-PCR). For the specificity of regeneration mechanism with P. euphratica, large amount of DEGs involved in "plant-pathogen interaction", ubiquitin-26S proteosome mediated proteolysis pathway, stress-responsive DEGs, and senescence-associated DEGs were summarized to possibly account for the differentiation difference with distinct genotypes of P. euphratica. The result in this study helps screening of key regulators in mediating the shoot differentiation. The transcriptomic characteristic in P. euphratica further enhances our understanding of key processes affecting the regeneration capacity of de novo shoots among distinct species.

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“…For example, out of the SASPs, IL-6, IL-8, and CCL2 enhance tumor cell proliferation [14,121]; VEGF promotes angiogenesis [122]; IL-6, IL-8, IGFBP7, and PAI-1 augment senescence [119][120][121][122][123][124]. It was reported that the multifunctional cytokines such as TGF-β family ligands, CCL2, and VEGF evoke cellular senescence [125] while PDGF-AA promotes wound healing [11,126]. In senescent cells, many of the SASP factors discussed above are activated at the transcriptional level [119,120,127].…”

Section: Cellular Senescence and The Role Of Saspsmentioning

confidence: 99%

The Emerging Role of Senescence in Ocular Disease

Sreekumar

Hinton

Kannan

2020

Oxidative Medicine and Cellular Longevity

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Cellular senescence is a state of irreversible cell cycle arrest in response to an array of cellular stresses. An important role for senescence has been shown for a number of pathophysiological conditions that include cardiovascular disease, pulmonary fibrosis, and diseases of the skin. However, whether senescence contributes to the progression of age-related macular degeneration (AMD) has not been studied in detail so far and the present review describes the recent research on this topic. We present an overview of the types of senescence, pathways of senescence, senescence-associated secretory phenotype (SASP), the role of mitochondria, and their functional implications along with antisenescent therapies. As a central mechanism, senescent cells can impact the surrounding tissue microenvironment via the secretion of a pool of bioactive molecules, termed the SASP. An updated summary of a number of new members of the ever-growing SASP family is presented. Further, we introduce the significance of mechanisms by which mitochondria may participate in the development of cellular senescence. Emerging evidence shows that extracellular vesicles (EVs) are important mediators of the effects of senescent cells on their microenvironment. Based on recent studies, there is reasonable evidence that senescence could be a modifiable factor, and hence, it may be possible to delay age-related diseases by modulating basic aging mechanisms using SASP inhibitors/senolytic drugs. Thus, antisenescent therapies in aging and age-related diseases appear to have a promising potential.

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Cellular senescence in development, regeneration and disease

Cited by 210 publications

References 124 publications

Interactions between Muscle and Bone—Where Physics Meets Biology

Interactions between Muscle and Bone—Where Physics Meets Biology

Identification of Shoot Differentiation-Related Genes in Populus euphratica Oliv.

The Emerging Role of Senescence in Ocular Disease

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