Myofibroblast specific targeting approaches to improve fibrosis treatment

Elfa Beaven, Raj Kumar, Himanshu N. Bhatt, Stephanie V. Esquivel, Md Nurunnabi

Research output: Contribution to journalArticlepeer-review

9 Scopus citations

Abstract

Fibrosis has been shown to develop in individuals with underlying health conditions, especially chronic inflammatory diseases. Fibrosis is often diagnosed in various organs, including the liver, lungs, kidneys, heart, and skin, and has been described as excessive accumulation of extracellular matrix that can affect specific organs in the body or systemically throughout the body. Fibrosis as a chronic condition can result in organ failure and result in death of the individual. Understanding and identification of specific biomarkers associated with fibrosis has emerging potential in the development of diagnosis and targeting treatment modalities. Therefore, in this review, we will discuss multiple signaling pathways such as TGF-β, collagen, angiotensin, and cadherin and outline the chemical nature of the different signaling pathways involved in fibrogenesis as well as the mechanisms. Although it has been well established that TGF-β is the main catalyst initiating and driving multiple pathways for fibrosis, targeting TGF-β can be challenging as this molecule regulates essential functions throughout the body that help to keep the body in homeostasis. We also discuss collagen, angiotensin, and cadherins and their role in fibrosis. We comprehensively discuss the various delivery systems used to target collagen, angiotensin, and cadherins to manage fibrosis. Nevertheless, understanding the steps by which this molecule drives fibrosis development can aid in the development of specific targets of its cascading mechanism. Throughout the review, we will demonstrate the mechanism of fibrosis targeting to improve targeting delivery and therapy.

Original languageEnglish
Pages (from-to)13556-13571
Number of pages16
JournalChemical Communications
Volume58
Issue number98
DOIs
StatePublished - 8 Dec 2022
Externally publishedYes

Bibliographical note

Publisher Copyright:
© 2022 The Royal Society of Chemistry.

Funding

We acknowledge funding by the Cancer Prevention Research Institute of Texas (CPRIT) through Texas Regional Excellence in Cancer Award (TREC) under Award No. PR210153, and the National Institutes of Health (NIH) under Award No. R03OD032624. The contents of this paper are solely the authors' responsibility and do not necessarily represent the official views of NIH.

FundersFunder number
Texas Regional Excellence in Cancer AwardPR210153
National Institutes of Health
NIH Office of the DirectorR03OD032624
Cancer Prevention and Research Institute of Texas

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