Vikas Jain*
Hepatic stellate cells (HSCs) are phenotypically active and develop a phenotype resembling myofibroblasts in the perisinusoidal region of the liver. Affected hepatic function, portal hypertension, increased vascular resistance; fibrosis, cirrhosis, and hepatocellular carcinoma are all results of this phenotypic transformation, which is also responsible for the accumulation and production of various extracellular matrix (ECM) proteins in the perisinusoidal space. In the injured liver, the main collagen-producing cells are activated HSCs/myofibroblasts. As a result, HSCs are frequently the focus of fibrosis treatments. Since HSCs contain the majority of the body's retinol, antifibrotic nanomedicine frequently target them with vitamin A decorating. Transforming growth factor-beta, collagen, and connective tissue growth factors are targeted by vitamin A-decorated nanomedicine with siRNAs to reduce fibrosis by inhibiting fibrogenesis and the expression of genes linked with the extracellular matrix (ECM).
Numerous miRNAs also have pro- and antifibrotic properties. Profibrotic and antifibrotic miRNAs are targeted in the fibrotic liver using their corresponding antagomirs and agomirs, respectively, together with HSC-specific Nano decoration. By inhibiting the expression of genes linked to the ECM, these miRNA therapies lower fibrogenesis. However, the activation of a distinct class of profibrotic signalling pathways linked to ECM build-up in the fibrotic liver is what causes liver fibrosis. Therefore, suppressing individual genes with siRNAs or specifically targeting miRNA may not be able to alleviate fibrosis to a higher level. To transport medications to activated HSCs in the wounded liver, however, nanodecorating of a drug is helpful. The focus of this review will be on targeted drug delivery to activated HSCs in the liver that has sustained long-term damage.
KeywordsDrug Delivery; Fibrotic Liver; Nanomedicine; Hepatic stellate cells; Nano-Based; Nanotechnology
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