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Mechanobiology is an emerging field of science at the interface of biology, engineering, and physics that focuses on how physical forces and changes in the mechanical properties of cells and tissues contribute to development, cell differentiation, physiology, and disease.[1] A major challenge in the field is understanding mechanotransduction—the molecular mechanisms by which cells sense and respond to mechanical signals.

While medicine has typically looked for the genetic and biochemical basis of disease, advances in mechanobiology suggest that changes in cell mechanics, extracellular matrix structure, or mechanotransduction may contribute to the development of many diseases, including atherosclerosis, fibrosis, asthma, osteoporosis, heart failure, and cancer[2][3]. There is also a strong mechanical basis for many generalized medical disabilities, such as lower back pain, foot and postural injury, deformity, and irritable bowel syndrome.[citation needed]

The effectiveness of many of the mechanical therapies already in clinical use shows how important physical forces can be in physiological control. For example, pulmonary surfactant promotes lung development in premature infants; modifying the tidal volumes of mechanical ventilators reduces morbidity and death in patients with acute lung injury; expandable stents physically prevent coronary artery constriction; tissue expanders increase the skin area available for reconstructive surgery;[4] and surgical tension application devices are used for bone fracture healing, orthodontics, cosmetic breast expansion and closure of non-healing wounds.[citation needed]

Insights into the mechanical basis of tissue regulation may also lead to development of improved medical devices, biomaterials, and engineered tissues for tissue repair and reconstruction.[5]

Stretch-activated ion channels, caveolae, integrins, cadherins, growth factor receptors, myosin motors, cytoskeletal filaments, nuclei, extracellular matrix, and numerous other molecular structures and signaling molecules have been shown to contribute to cellular mechanotransduction. In addition, endogenous cell-generated traction forces contribute significantly to these responses by modulating tensional prestress within cells, tissues, and organs that govern their mechanical stability, as well as mechanical signal transmission from the macroscale to the nanoscale.[6][7]

It is claimed all cells are mechanosensitive.[8] Collectively cells respond to perturbations to their local mechanical environment resulting in tissue-level observations. For example, at the tissue-level an artery will either thicken or thin in response to changes in blood pressure above or below the healthy levels.[9][10] That is, in the case of increased blood pressure (Hypertension) individual arterial cells experience greater circumferential stress (or tension). In order to alleviate this tension, they produce growth factors, which in turn stimulates proliferation. The net result is increased arterial wall thickness but the stress levels in the artery are restored to the normal levels.[11]

Using mankind as a macroscopic example, in closed chain function, ground reactive forces, a dynamic architecture and a dynamic equilibrium of forces around joint axes impact the posture to produce tissue stress. This tissue stress can be both beneficial or harmful. Since gravity, hard, unyielding ground surfaces and other factors such as activity level, body weight and health state impact each of us differently there is no one plan of care that will work for every individual. This results in a lifetime of adaptation of tissues via Wolff's and Davis' Laws of Bone and Soft Tissue respectively that can unless compensated and/or corrected lead to breakdown, injury and reduced quality of life on a case to case basis.

As a further example, the foot has an inherited functional shape which when used will remodel and adapt in predictable manners. Theoretically programs can be establishing for prevention, performance enhancement and quality of life upgrading in addition to the treatment of pathology and pain. These interventions, some day, will cause positive remodeling of bone and soft tissue that will extend and possibly improve the mechanobiological timeline of mankind.

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Scientific journals[edit]


  1. ^ Jacobs, Christopher R.; Huang, Hayden; Kwon, Ronald Y. (2012). Introduction to Cell Mechanics and Mechanobiology. Garland Science. ISBN 978-0824798512.
  2. ^ Spill, F.; Reynolds, D.S.; Kamm, R.D.; Zaman, M.H. (2016). "Impact of the physical microenvironment on tumor progression and metastasis". Current Opinion in Biotechnology. 40: 41–48. doi:10.1016/j.copbio.2016.02.007. PMC 4975620. PMID 26938687.
  3. ^ Spill, Fabian; Bakal, Chris; Mak, Michael (2018). "Mechanical and Systems Biology of Cancer". Computational and Structural Biotechnology Journal. 16: 237–245. doi:10.1016/j.csbj.2018.07.002. PMC 6077126. PMID 30105089.
  4. ^ Buganza Tepole, A; Ploch, CJ; Wong, J; Gosain, AK; Kuhl, E (2011). "Growing skin - A computational model for skin expansion in reconstructive surgery". J. Mech. Phys. Solids. 59 (10): 2177–2190. doi:10.1016/j.jmps.2011.05.004. PMC 3212404. PMID 22081726.
  5. ^ Ingber, DE (2003). "Mechanobiology and diseases of mechanotransduction". Annals of Medicine. 35 (8): 564–77. doi:10.1080/07853890310016333. PMID 14708967.
  6. ^ Ingber, DE (1997). "Tensegrity: the architectural basis of cellular mechanotransduction". Annu. Rev. Physiol. 59: 575–599. doi:10.1146/annurev.physiol.59.1.575. PMID 9074778.
  7. ^ Ingber, DE (2006). "Cellular mechanotransduction: putting all the pieces together again". FASEB J. 20 (7): 811–827. doi:10.1096/fj.05-5424rev. PMID 16675838.
  8. ^ Kung, C (4 August 2005). "A possible unifying principle for mechanosensation". Nature. 436 (7051): 647–54. doi:10.1038/nature03896. PMID 16079835.
  9. ^ Hayenga, HN; Hu, JJ; Meyer, CA; Wilson, E; Hein, TW; Kuo, L; Humphrey, JD (2012). "Differential progressive remodeling of coronary and cerebral arteries and arterioles in an aortic coarctation model of hypertension". Frontiers in Physiology. 3: 420. doi:10.3389/fphys.2012.00420. PMC 3495262. PMID 23162468.
  10. ^ Humphrey, JD (August 2008). "Mechanisms of arterial remodeling in hypertension: coupled roles of wall shear and intramural stress". Hypertension. 52 (2): 195–200. doi:10.1161/hypertensionaha.107.103440. PMC 2753501. PMID 18541735.
  11. ^ Thorne, BC; Hayenga, HN; Humphrey, JD; Peirce, SM (2011). "Toward a multi-scale computational model of arterial adaptation in hypertension: verification of a multi-cell agent based model". Frontiers in Physiology. 2: 20. doi:10.3389/fphys.2011.00020. PMC 3118494. PMID 21720536.

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