Challenges and opportunities of medicines for treating tendon inflammation and fibrosis: A comprehensive and mechanistic review

Author:

Najafi Zohreh1,Rahmanian‐Devin Pouria2,Baradaran Rahimi Vafa3ORCID,Nokhodchi Ali45,Askari Vahid Reza1ORCID

Affiliation:

1. Applied Biomedical Research Center Mashhad University of Medical Sciences Mashhad Iran

2. Department of Pharmaceutics, School of Pharmacy Mashhad University of Medical Sciences Mashhad Iran

3. Department of Cardiovascular Diseases, Faculty of Medicine Mashhad University of Medical Sciences Mashhad Iran

4. Lupin Pharmaceutical Research Center 4006 NW 124th Ave., Coral Springs Florida Florida 33065 USA

5. Pharmaceutics Research Laboratory, School of Life Sciences University of Sussex Brighton BN1 9QJ UK

Abstract

AbstractBackgroundTendinopathy refers to conditions characterized by collagen degeneration within tendon tissue, accompanied by the proliferation of capillaries and arteries, resulting in reduced mechanical function, pain, and swelling. While inflammation in tendinopathy can play a role in preventing infection, uncontrolled inflammation can hinder tissue regeneration and lead to fibrosis and impaired movement.ObjectivesThe inability to regulate inflammation poses a significant limitation in tendinopathy treatment. Therefore, an ideal treatment strategy should involve modulation of the inflammatory process while promoting tissue regeneration.MethodsThe current review article was prepared by searching PubMed, Scopus, Web of Science, and Google Scholar databases. Several treatment approaches based on biomaterials have been developed.ResultsThis review examines various treatment methods utilizing small molecules, biological compounds, herbal medicine‐inspired approaches, immunotherapy, gene therapy, cell‐based therapy, tissue engineering, nanotechnology, and phototherapy.ConclusionThese treatments work through mechanisms of action involving signaling pathways such as transforming growth factor‐beta (TGF‐β), mitogen‐activated protein kinases (MAPKs), and nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NF‐κB), all of which contribute to the repair of injured tendons.

Publisher

Wiley

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