Complete regeneration of damaged tissues/organs has always been the ultimate challenge in regenerative medicine. Aging has long been considered the basis of age-related diseases, as senescent cells gradually accumulate in tissues with increasing age, tissues exhibit aging and normal physiological functions are inhibited. In recent years, in damaged tissues, scholars have found that the number of cells with features of cellular senescence continues to increase over time. The accumulation of senescent cells severely hinders the healing of damaged tissues. Furthermore, by clearing senescent cells or inhibiting the aging microenvironment, damaged tissues regained their original regenerative and repair capabilities. On the other hand, various biomaterials have been proved to have good biocompatibility and can effectively support cell regeneration after injury. Combining the two solutions, inhibiting the cellular senescence in damaged tissues and establishing a pro-regenerative environment through biomaterial technology gradually reveals a new, unexpected treatment strategy applied to the field of regenerative medicine. In this review, we first elucidate the main characteristics of senescent cells from morphological, functional and molecular levels, and discuss in detail the process of accumulation of senescent cells in tissues. Then, we will explore in depth how the accumulation of senescent cells after damage affects tissue repair and regeneration at different stages. Finally, we will turn to how to promote tissue regeneration and repair in the field of regenerative medicine by inhibiting cellular senescence combined with biomaterial technology. Our goal is to understand the relationship between cellular senescence and tissue regeneration through this new perspective, and provide valuable references for the development of new therapeutic strategies in the future.
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http://dx.doi.org/10.1002/SMMD.20230030 | DOI Listing |
Clin Transl Med
January 2025
Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Background: Sporadic aortic aneurysm and dissection (AAD) is a critical condition characterised by the progressive loss of vascular smooth muscle cells (VSMCs) and the breakdown of the extracellular matrix. However, the molecular mechanisms responsible for the phenotypic switch and loss of VSMCs in AAD are not fully understood.
Methods And Results: In this study, we employed a discovery-driven, unbiased approach.
Aging Cell
December 2024
Department of Cell Biology, Neurobiology and Anatomy, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
Despite advances in understanding molecular and cellular changes in the aging nervous system, the upstream drivers of these changes remain poorly defined. Here, we investigate the roles of non-neural tissues in neuronal aging, using the cutaneous PVD polymodal sensory neuron in Caenorhabditis elegans as a model. We demonstrate that during normal aging, PVD neurons progressively develop excessive dendritic branching, functionally correlated with age-related proprioceptive deficits.
View Article and Find Full Text PDFImmun Ageing
December 2024
Université Paris Cité, INSERM, PARCC, Paris, France.
Background: Immune ageing complicates cancer treatment in older individuals. While immunotherapy targeting the PD-1/PD-L1 pathway can reinvigorate T cells, these cells tend to become senescent with age. This study investigates different CD8 T cell subsets usually associated with senescence, in cancer patients over 70 years old who are undergoing anti-PD-1/PD-L1 immunotherapy, and examines the relationship between these senescent cells and prior chemotherapy exposure.
View Article and Find Full Text PDFGeroscience
December 2024
Department of Ecology, Evolution, and Marine Biology, Department of Molecular, Cellular, and Cell Biology, Neuroscience Research Institute, University of California, Santa Barbara, CA, 93106, USA.
Significant links between aging and DNA methylation are emerging from recent studies. On the one hand, DNA methylation undergoes changes with age, a process termed as epigenetic drift. On the other hand, DNA methylation serves as a readily accessible and accurate biomarker for aging.
View Article and Find Full Text PDFNat Aging
December 2024
Université Côte d'Azur, Centre National de la Recherche Scientifique (CNRS) UMR7284, Institut National de la Santé et de la Recherche Médicale (INSERM) U1081, Institute for Research on Cancer and Aging, Nice (IRCAN), Nice, France.
Although senescent cells can be eliminated by the immune system, they tend to accumulate with age in various tissues. Here we show that senescent cells can evade immune clearance by natural killer (NK) cells by upregulating the expression of the disialylated ganglioside GD3 at their surface. The increased level of GD3 expression on senescent cells that naturally occurs upon aging in liver, lung, kidney or bones leads to a strong suppression of NK-cell-mediated immunosurveillance.
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