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β2-adrenoceptors kick osteoarthritis - Time to rethink prevention and therapy
Zsuzsa Jenei-Lanzl1, Rainer H Straub2
1Dr. Rolf M. Schwiete Research Unit for Osteoarthritis, Department of Trauma Surgery and Orthopedics, Goethe University Frankfurt, University Hospital, Frankfurt am Main, Germany.
Abstract:
Although, during the past decades, substantial advances emerged in identifying major local and systemic factors contributing to initiation and progression of osteoarthritis (OA), some neuroendocrine mechanisms are still not understood or even neglected when thinking about novel therapeutic options. One of which is the sympathetic nervous system that exhibits various OA-promoting effects in different tissues of the joint. Interestingly, the β2-adrenoceptor (AR) mediates the majority of these effects as demonstrated by several in vitro, in vivo as well as in clinical studies. This review article does not only summarize studies of the past two decades demonstrating that the β2-AR plays an OA-promoting role in different tissues of the joint but also aims to encourage the reader to think about next-level research to discover novel and innovative preventive and/or therapeutic strategies targeting the β2-AR in OA.
Insights
The sympathetic nervous system, particularly the β2-adrenoceptor (AR), promotes osteoarthritis (OA). Targeting β2-AR offers potential for novel OA therapies.
Area of Science:
- Neuroendocrinology
- Rheumatology
- Pharmacology
Background:
- Osteoarthritis (OA) pathogenesis involves local and systemic factors, with neuroendocrine mechanisms often overlooked.
- The sympathetic nervous system (SNS) plays a significant role in OA progression.
- The β2-adrenoceptor (AR) is a key mediator of SNS-driven OA effects.
Purpose of the Study:
- To review the OA-promoting role of the β2-adrenoceptor (AR) over the past two decades.
- To highlight the involvement of the SNS and β2-AR in joint tissues affected by OA.
- To stimulate research into novel therapeutic strategies targeting the β2-AR for OA prevention and treatment.
Main Methods:
- Literature review of in vitro, in vivo, and clinical studies.
- Analysis of research on sympathetic nervous system involvement in osteoarthritis.
- Synthesis of findings related to β2-adrenoceptor function in OA.
Main Results:
- Evidence confirms the β2-adrenoceptor mediates significant OA-promoting effects in joint tissues.
- Multiple studies demonstrate the role of β2-AR in OA initiation and progression.
- The SNS, via β2-AR, influences various components of the OA joint.
Conclusions:
- The β2-adrenoceptor is a critical factor in osteoarthritis pathogenesis.
- Targeting the β2-adrenoceptor presents a promising avenue for developing new OA treatments.
- Further research is warranted to explore innovative therapeutic strategies focused on the β2-AR pathway in OA.
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