These variations significantly influence the role of GLP-1 in regulating islet function and glucose homeostasis.131 Research indicates that the expression level of GLP-1R on -cells is relatively low.131 Although GLP-1Rs are present, they are limited in number, making the direct inhibitory effect of GLP-1 on -cells relatively weak.247 The primary action often occurs through indirect mechanisms, such as insulin and somatostatin.244 Conversely, the expression level of GLP-1R on -cells is relatively high.248 GLP-1 can effectively bind to receptors on -cells, stimulating the secretion of somatostatin.248 As a broad-spectrum inhibitory hormone, somatostatin can effectively inhibit glucagon secretion from -cells and insulin secretion from -cells.249,250 Relevant studies suggest that the expression of GLP-1R on -cells is crucial for GLP-1s regulation of somatostatin secretion and the overall inhibitory effect on glucagon.248,251,252 This mechanism is particularly evident in the use of GLP-1-based drugs, such as GLP-1RAs, in the treatment of T2DM
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Additionally, given the presence and adverse effects of the local tissue reninangiotensin system (tRAS) in discs, whether ANP has a protective impact via suppressing the tRAS in IVDD is an interesting avenue for future research (147149)
Senescent cells can remodel the microenvironment by secreting various cytokines, growth factors, chemokines, and senescence-associated secretory phenotypes (SASPs), ultimately leading to the development of malignant tumour development (224, 225)
