Abstract
The salivary gland (SG) microvasculature constitutes a dynamic cellular organization instrumental to preserving tissue stability and homeostasis. The interplay between pericytes (PCs) and endothelial cells (ECs) culminates as a key ingredient that coordinates the development, maturation, and integrity of vessel building blocks. PCs, as a variety of mesenchymal stem cells, enthrall in the field of regenerative medicine, supporting the notion of regeneration and repair. PC-EC interconnections are pivotal in the kinetic and intricate process of angiogenesis during both embryological and post-natal development. The disruption of this complex interlinkage corresponds to SG pathogenesis, including inflammation, autoimmune disorders (Sjögren’s syndrome), and tumorigenesis. Here, we provided a global portrayal of major signaling pathways between PCs and ECs that cooperate to enhance vascular steadiness through the synergistic interchange. Additionally, we delineated how the crosstalk among molecular networks affiliate to contribute to a malignant context. Additionally, within SG microarchitecture, telocytes and myoepithelial cells assemble a labyrinthine companionship, which together with PCs appear to synchronize the regenerative potential of parenchymal constituents. By underscoring the intricacy of signaling cascades within cellular latticework, this review sketched a perceptive basis for target-selective drugs to safeguard SG function.
Highlights
The salivary gland (SG) microvasculature represents a kinetic cellular system, crucial for maintaining tissue vitality and homeostasis
The activation of the canonical pathway is appointed to double concomitant proteolytic cleavages of NOTCH receptors by two enzymes: an A-disintegrin and metalloprotease (ADAM) and gammasecretase in the sight of Presenilin 1 and 2 (PS1/2) [98]. These contingencies lead to the release of Notch intracellular domain (NICD) [97,99–101] which disentangles from the plasma membrane and goes ahead to the nucleus where it connects with the transcriptional repressor CBF1/suppressor of hairless/LAG1 (CSL) (CBF1/Suppressor of hairless/LAG1 or RBPJ kappa)
Pericyte-endotelial cell (PC-endothelial cells (ECs)) interconnections are instrumental for vascular development, maturation, and remodeling in both physiological and pathological conditions
Summary
The salivary gland (SG) microvasculature represents a kinetic cellular system, crucial for maintaining tissue vitality and homeostasis. PCs play a well-documented role in the dynamic and intricate process of angiogenesis, defined as the proliferation of ECs, sprouting, constitution, and branching of new vessels from pre-existing ones in order to establish interlinking capillary networks by mechanical support and paracrine factors [3,6,9–14] Dysfunction of this comprehensive interconnection parallels the pathogenesis of SG disorders [15,16]. Several diseases and stress conditions, such as inflammation and ischemia, autoimmune background (Sjögren’s syndrome), and post-radiotherapy in neoplastic contexture result in the disorganizing of SG microarchitecture [3,18,19] These phenomena are ascribed to acinar cells atrophy, apoptosis, and uncontrolled progression of fibrosis and lead to SG dysfunction (hyposalivation, xerostomia), thereby exacerbating some of the pathological processes [20,21]. One of the most used membranebound markers is NG2 (neural/glial antigen 2) [25], together with alanine aminopeptidase (CD13) and CD90 [2,25] Another cytosolic marker useful in PCs identification is alphasmooth muscle actin (alpha SMA) [26], related to modulating the blood flow [1,3]. This review highlighted a global picture of a complex interaction network of crosstalk among signaling pathways between PCs and ECs, expressing synergistic reciprocity that delineates a rational basis for different pathogenetic elements as therapeutic targets in SG diseases
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
