Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Editorial
. 2017 Jul;51(13):989-990.
doi: 10.1136/bjsports-2017-097634.

Become one with the force: optimising mechanotherapy through an understanding of mechanobiology

Stuart J Warden  1 , William R Thompson  1
Affiliations
Editorial

Become one with the force: optimising mechanotherapy through an understanding of mechanobiology

Stuart J Warden et al. Br J Sports Med. 2017 Jul.
No abstract available

Keywords: Exercise; Injury prevention; Molecular; Physical activity; Physical stress.

PubMed Disclaimer

Conflict of interest statement

Competing interests: None declared.

Figures

Figure 1
Figure 1
Mechanical forces direct cellular activities to induce tissue adaptation. Extrinsically and intrinsically generated mechanical forces load musculoskeletal tissues, with the characteristics of the resultant tissue forces being dependent on the ability of the tissue to resist those forces. Tissue forces are transmitted to the micromechanical environment of resident cells, with cellular mechanical properties influencing the characteristics of the cellular forces. Cells can modify their micromechanical environment via cytoskeletal rearrangement, which feedbacks to alter cellular sensitivity to incoming forces. When cellular forces are sufficient, the cell initiates a molecular response, which ultimately alters synthesis and/or degradation of the extracellular matrix. The latter alters tissue mechanical properties, which feeds back to influence tissue forces. (Reprinted from Thompson et al, by permission of Oxford University Press and the American Physical Therapy Association.)
Figure 2
Figure 2
A variety of extracellular receptors activate an overlapping network of mechanosensitive pathways. (A) Musculoskeletal cells can sense incoming mechanical signals using a diverse group of transmembrane mechanosensitive proteins (‘mechanosensors’), including stretch-activated ion channels, cell-membrane spanning G protein-coupled receptors, growth-factor receptors and integrins. The mechanical stimulation of these proteins can lead to changes in their affinity to binding partners or ion conductivity. (B) Mechanical stimulation of the mechanosensors and alteration in their binding capacity or ion conductivity converts the mechanical signal into a biochemical signal (‘biochemical coupling’) triggering intracellular signalling cascades. Many of the pathways overlap sharing signalling molecules. The convergence of the pathways results in the activation of select transcription factors, including nuclear factor of activated T cells, nuclear factor-κβ, activator protein 1, GATA4 (a member of the transcription factor family characterised by the ability to bind the DNA sequence ‘GATA’) and signal transducer and activator of transcription factors. The transcription factors translocate to the nucleus and modulate the expression of a panel of mechanosensitive genes, including early growth response 1, lex1, Fos, Jun and cyclooxygenase-2. Ultimately, the net sum of gene-expression reprogramming determines the functional response of the cell to a mechanical stimulus. Akt/PKB, protein kinase B; AP1, activator protein 1; CaMK, calcium/calmodulin-dependent kinase; Cox2, cyclooxygenase-2; DAG, diacyl-glycerol; Egr1, early growth response 1; ERK, extracellular signal-regulated kinase; FAK, focal adhesion kinase; IP3, inositol triphosphate; JNKs, c-Jun N-terminal kinases; MEK, mitogen-activated protein kinase; MEKK, mitogen-activated protein kinase kinase; MLCK, myosin light-chain kinase; NFAT, nuclear factor of activated T cells; NF-κβ, nuclear factor-κβ; NO, nitric oxide; NOS, nitric oxide synthase; PAK, p21-activated kinase; PI3K, phosphoinositide 3-kinase; PKC, protein kinase C; PLC, phospholipase C; Raf, rapidly accelerated fibrosarcoma kinase; Ras, rat sarcoma small GTPase; STATs, signal transducer and activator of transcription factors. (Reprinted from Thompson et al, by permission of Oxford University Press and the American Physical Therapy Association.)
See this image and copyright information in PMC

Comment on

  • Br J Sports Med.

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Thompson WR, Scott A, Loghmani MT, et al. Understanding Mechanobiology: physical therapists as a force in Mechanotherapy and musculoskeletal regenerative Rehabilitation. Phys Ther. 2016;96:560–9. - PMC - PubMed
    1. Khan KM, Scott A. Mechanotherapy: how physical therapists’ prescription of exercise promotes tissue repair. Br J Sports Med. 2009;43:247–52. - PMC - PubMed
    1. Ingber DE. Mechanobiology and diseases of mechanotransduction. Ann Med. 2003;35:564–77. - PubMed
    1. Robling AG, Castillo AB, Turner CH. Biomechanical and molecular regulation of bone remodeling. Annu Rev Biomed Eng. 2006;8:455–98. - PubMed
    1. Huisman E, Lu A, McCormack RG, et al. Enhanced collagen type I synthesis by human tenocytes subjected to periodic in vitro mechanical stimulation. BMC Musculoskelet Disord. 2014;15:386. - PMC - PubMed

Publication types