Pathophysiologic implications and therapeutic potentials of telocytes in multiorgan fibrosis

Telocytes (TCs) are unique stromal cells with distinctive morphology, ultrastructural features, and intercellular communication abilities. Accumulating evidence supports their critical roles in tissue homeostasis, regeneration, and stem cell niche maintenance through both cell-to-cell contacts and delivery of paracrine signals. The purpose of this review is to provide an up-to-date overview of the current knowledge regarding the pathophysiologic implications and therapeutic potentials of TCs in multiorgan fibrosis.

Loss and/or structural degeneration of TCs have been implicated in the pathogenesis of fibrotic conditions affecting the skin, gastrointestinal tract, heart, lungs, kidneys, and reproductive organs. TC depletion has often been associated with extracellular matrix remodeling, aberrant fibroblast activation, disruption of stem cell support, and altered tissue architecture. Experimental evidence suggests that TCs may possess antifibrotic therapeutic potentials, with TC transplantation or administration of TC-derived secretome/extracellular vesicles mitigating fibrosis progression in different preclinical models.

TCs are emerging as pivotal regulators of stromal homeostasis across several organs and their loss appears to be a unifying feature in the pathogenesis of tissue fibrosis in different anatomical districts. Targeting TCs, either by preserving their function or restoring their networks/paracrine signals, may open new therapeutic avenues for managing various fibrotic diseases.