The role of cellular senescence in tissue repair and regeneration.

Published on Jun 25, 2021in Mechanisms of Ageing and Development4.304
· DOI :10.1016/J.MAD.2021.111528
Lucía Antelo-Iglesias1
Estimated H-index: 1
Pilar Picallos-Rabina3
Estimated H-index: 3
+ 2 AuthorsManuel Collado35
Estimated H-index: 35
Abstract null null The capacity to regenerate damaged or lost tissue varies widely along the animal kingdom and generally declines with aging of the organism. The gradual accumulation of senescent cells in tissues during aging has been causally involved in their reduced function at old age, and to be at the basis of age-related diseases. Recently, however, cellular senescence has been shown to play a positive role as a morphogenetic force modelling and promoting tissue development during embryogenesis, and to be responsible for tissue wound healing and repair. Work done on organismal models ranging from fish and amphibians, with extraordinary regenerative capacities, to mammals, with a more restricted regenerative potential, is shedding light on a novel and unexpected function of cellular senescence. In this review, we will analyze the senescence phenotype and how could it be contributing or restricting tissue regeneration.
📖 Papers frequently viewed together
#1Katie J. Mylonas (Edin.: University of Edinburgh)H-Index: 10
#2Eoin O'Sullivan (Edin.: University of Edinburgh)H-Index: 16
Last. David A. Ferenbach (Edin.: University of Edinburgh)H-Index: 19
view all 13 authors...
The ability of the kidney to regenerate successfully after injury is lost with advancing age, chronic kidney disease, and after irradiation. The factors responsible for this reduced regenerative capacity remain incompletely understood, with increasing interest in a potential role for cellular senescence in determining outcomes after injury. Here, we demonstrated correlations between senescent cell load and functional loss in human aging and chronic kidney diseases including radiation nephropathy...
5 CitationsSource
#1Tatiana Kisseleva (UCSD: University of California, San Diego)H-Index: 45
#2David A. Brenner (UCSD: University of California, San Diego)H-Index: 149
Chronic liver injury leads to liver inflammation and fibrosis, through which activated myofibroblasts in the liver secrete extracellular matrix proteins that generate the fibrous scar. The primary source of these myofibroblasts are the resident hepatic stellate cells. Clinical and experimental liver fibrosis regresses when the causative agent is removed, which is associated with the elimination of these activated myofibroblasts and resorption of the fibrous scar. Understanding the mechanisms of ...
32 CitationsSource
#1Caizhen LiH-Index: 1
#2Yanting ShenH-Index: 1
Last. Jun WangH-Index: 6
view all 5 authors...
Acute kidney injury (AKI) is a common clinical problem, and patients who survive AKI have a high risk of chronic kidney disease (CKD). The mechanism of CKD post-AKI, characterized by progressive renal fibrosis, is still unclear. Maladaptive tubular epithelial cells (TECs) after AKI are considered a leading cause of renal fibrosis post-AKI. TECs under maladaptive repair manifest characteristics of senescence. Removing senescent TECs by genetic ablation has been proven effective in reducing renal ...
2 CitationsSource
#1Diogo Paramos-de-Carvalho (NOVA: Universidade Nova de Lisboa)H-Index: 1
#2Isaura Martins (IMM: Instituto de Medicina Molecular)H-Index: 2
Last. Leonor Saúde (IMM: Instituto de Medicina Molecular)H-Index: 14
view all 10 authors...
SUMMARY Persistent senescent cells (SCs) are known to underlie ageing-related chronic disorders, but it is now recognized that SCs may be at the center of tissue remodeling events, namely during development or organ repair. Here we show that two distinct senescence profiles are induced in the context of a spinal cord injury between the regenerating zebrafish and the non-regenerating mouse. While induced-SCs in the zebrafish are progressively cleared out, they accumulate over time in mice. Deplet...
4 CitationsSource
#1Ryo Takahashi (Ochanomizu University)H-Index: 15
#1R. Takahashi (Ochanomizu University)H-Index: 1
Last. Eiji SaitohH-Index: 76
view all 7 authors...
Hydrodynamic motion can generate a flux of electron-spin’s angular momentum via the coupling between fluid rotation and electron spins. Such hydrodynamic generation, called spin hydrodynamic generation (SHDG), has recently attracted attention in a wide range of fields, especially in spintronics. Spintronics deals with spin-mediated interconversion taking place on a micro or nano scale because of the spin-diffusion length scale. To be fully incorporated into the interconversion, SHDG physics shou...
15 CitationsSource
#1Marie Helena Docherty (Edin.: University of Edinburgh)H-Index: 1
#2David P. Baird (Edin.: University of Edinburgh)H-Index: 2
Last. David A. Ferenbach (Edin.: University of Edinburgh)H-Index: 19
view all 4 authors...
Cellular senescence refers to a cellular phenotype characterised by an altered transcriptome, pro-inflammatory secretome and generally irreversible growth arrest. Acutely senescent cells are widely recognised as performing key physiological functions in vivo promoting normal organogenesis, successful wound repair and cancer defence. In contrast, the accumulation of chronically senescent cells in response to aging, cell stress, genotoxic damage and other injurious stimuli is increasingly recognis...
13 CitationsSource
#1Birgit RitschkaH-Index: 3
#2Tania Knauer-MeyerH-Index: 1
Last. William M. KeyesH-Index: 16
view all 11 authors...
Young mammals possess a limited regenerative capacity in some tissues, which is lost upon maturation. We investigated whether cellular senescence might play a role in such loss during liver regeneration. We found that following partial hepatectomy, the senescence-associated genes p21, p16(Ink4a), and p19(Arf) become dynamically expressed in different cell types when regenerative capacity decreases, but without a full senescent response. However, we show that treatment with a senescence-inhibitin...
17 CitationsSource
#1Yuki Saito (Sapporo Medical University)H-Index: 5
#2Takako Chikenji (Sapporo Medical University)H-Index: 13
Last. Mineko Fujimiya (Sapporo Medical University)H-Index: 60
view all 5 authors...
Idiopathic inflammatory myopathies cause progressive muscle weakness and degeneration. Since high-dose glucocorticoids might not lead to full recovery of muscle function, physical exercise is also an important intervention, but some exercises exacerbate chronic inflammation and muscle fibrosis. It is unknown how physical exercise can have both beneficial and detrimental effects in chronic myopathy. Here we show that senescence of fibro-adipogenic progenitors (FAPs) in response to exercise-induce...
21 CitationsSource
#2Jorge Guerra-Varela (University of Santiago de Compostela)H-Index: 10
Last. Manuel ColladoH-Index: 35
view all 7 authors...
Cellular senescence is a stress response that limits the proliferation of damaged cells by establishing a permanent cell cycle arrest. Different stimuli can trigger senescence but excessive production or impaired clearance of these cells can lead to their accumulation during aging with deleterious effects. Despite this potential negative side of cell senescence, its physiological role as a pro-regenerative and morphogenetic force has emerged recently after the identification of programmed cell s...
22 CitationsSource
#1Marta Paez-Ribes (University of Cambridge)H-Index: 12
#2Estela González‐Gualda (University of Cambridge)H-Index: 3
Last. Daniel Muñoz-Espín (University of Cambridge)H-Index: 10
view all 4 authors...
Organismal ageing is a complex process driving progressive impairment of functionality and regenerative potential of tissues. Cellular senescence is a state of stable cell cycle arrest occurring in response to damage and stress and is considered a hallmark of ageing. Senescent cells accumulate in multiple organs during ageing, contribute to tissue dysfunction and give rise to pathological manifestations. Senescence is therefore a defining feature of a variety of human age‐related disorders, incl...
73 CitationsSource
Cited By0