The Potential Use of Cannabis in Tissue Fibrosis.

Nazar Pryimak,Olga Kovalchuk,Mariia Zaiachuk,Igor Kovalchuk

doi:10.3389/fcell.2021.715380

Nazar Pryimak, Olga Kovalchuk + Show 2 more

Open Access

https://doi.org/10.3389/fcell.2021.715380

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Abstract

Fibrosis is a condition characterized by thickening or/and scarring of various tissues. Fibrosis may develop in almost all tissues and organs, and it may be one of the leading causes of morbidity and mortality. It provokes excessive scarring that excels the usual wound healing response to trauma in numerous organs. Currently, very little can be done to prevent tissue fibrosis, and it is almost impossible to reverse it. Anti-inflammatory and immunosuppressive drugs are among the few treatments that may be efficient in preventing fibrosis. Numerous publications suggest that cannabinoids and extracts of Cannabis sativa have potent anti-inflammatory and anti-fibrogenic properties. In this review, we describe the types and mechanisms of fibrosis in various tissues and discuss various strategies for prevention and dealing with tissue fibrosis. We further introduce cannabinoids and their potential for the prevention and treatment of fibrosis, and therefore for extending healthy lifespan.

Highlights

Fibrosis is a pathology associated with the replacement of parenchyma with connective tissue during the healing process
When miR-30b-5p agomir was administered, it targeted Nod-like receptor family pyrin domain containing 3 (NLRP3) and mitigated liver inflammation. These results suggested that cannabinoid receptors 1 (CB1)/miR-30b-5p axis is able to modulate the activation of NLRP3 inflammasome and expression of NLRP3 in macrophages in liver inflammatory disease (Yang et al, 2020)
This study showed that AM1241 reduces fibrosis, by activating the cannabinoid 2 (CB2) receptor, and inhibiting TLR4/miR-155/NFκB p65 pathway (Ali et al, 2021)

Summary

Introduction

Fibrosis is a pathology associated with the replacement of parenchyma with connective tissue during the healing process. Abnormal wound healing resulting in scar formation includes similar phases/steps, such as inflammation, cell proliferation, and remodeling, but is characterized by more extensive deposition of collagen, fibrin, fibronectin, etc. Stimulation of inflammation and fibrosis, in part through TGF-β signaling pathway, activation of myofibroblasts and increased secretion of MMPs. Fibrosis enhancement through binding and activation of fibroblast growth factor receptor (FGFR).

Results

Conclusion