Effects of Nanomaterials on Synthesis and Degradation of the Extracellular Matrix.

Extracellular matrix (ECM) remodeling is accompanied by the continuous synthesis and degradation of the ECM components. This dynamic process plays an important role in guiding cell adhesion, migration, proliferation, and differentiation, as well as in tissue development, body repair, and maintenance of homeostasis. Nanomaterials, due to their photoelectric and catalytic properties and special structure, have garnered much attention in biomedical fields for use in processes such as tissue engineering and disease treatment. Nanomaterials can reshape the cell microenvironment by changing the synthesis and degradation of ECM-related proteins, thereby indirectly changing the behavior of the surrounding cells. This review focuses on the regulatory role of nanomaterials in the process of cell synthesis of different ECM-related proteins and extracellular protease. We discuss influencing factors and possible related mechanisms of nanomaterials in ECM remodeling, which may provide different insights into the design and development of nanomaterials for the treatment of ECM disorder-related diseases.

Impaired angiogenesis in ageing: the central role of the extracellular matrix.

Each step in angiogenesis is regulated by the extracellular matrix (ECM). Accumulating evidence indicates that ageing-related changes in the ECM driven by cellular senescence lead to a reduction in neovascularisation, reduced microvascular density, and an increased risk of tissue ischaemic injury. These changes can lead to health events that have major negative impacts on quality of life and place a significant financial burden on the healthcare system. Elucidating interactions between the ECM and cells during angiogenesis in the context of ageing is neceary to clarify the mechanisms underlying reduced angiogenesis in older adults. In this review, we summarize ageing-related changes in the composition, structure, and function of the ECM and their relevance for angiogenesis. Then, we explore in detail the mechanisms of interaction between the aged ECM and cells during impaired angiogenesis in the older population for the first time, discussing diseases caused by restricted angiogenesis. We also outline several novel pro-angiogenic therapeutic strategies targeting the ECM that can provide new insights into the choice of appropriate treatments for a variety of age-related diseases. Based on the knowledge gathered from recent reports and journal articles, we provide a better understanding of the mechanisms underlying impaired angiogenesis with age and contribute to the development of effective treatments that will enhance quality of life.