Mechanobiology is an emerging field of science at the interface of biology and engineering. It focuses on the way that physical forces and changes in cell or tissue mechanics contribute to development, physiology, and disease. A major challenge in the field is understanding mechanotransduction—the molecular mechanism by which cells sense and respond to mechanical signals.
While medicine has typically looked for the genetic 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. 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.
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; and surgical tension application devices are used for bone fracture healing, orthodontics, cosmetic breast expansion and closure of non-healing wounds.
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.
On a macroscopic level, Mechanobiology is poorly evidenced and remains mostly theoretical, experimental and computational. Using mankind as an 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.
Foundationally, as a further example, the foot has an inherited functional foot type, which when weighted, will remodel and adapt in predictable manners. Once foot typed, practitioners can interject, foot centering orthotics, muscle engine reactive forces and orthotic reactive forces non-operatively to position and engineer the foot in order to treat pain syndromes, deformity, degeneration and quality of life issues. 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.
Eventually, evidence will surface that will lead to paradigms of Mechanobiological diagnosis, treatment, maintenance and upgrading that will benefit various biological systems until then, Human Mechanobiology remains an intrapersonal medical, architectural and engineering field that requires a professional practitioner.
- Buganza Tepole A, Ploch CJ, Wong J, Gosain AK, Kuhl E. Growing skin - A computational model for skin expansion in reconstructive surgery. J. Mech. Phys. Solids, 2011;59:2177-2190.
- Ingber, DE. Mechanobiology and diseases of mechanotransduction. Annals of Medicine 2003; 35: 1-14
- Ingber DE. Tensegrity: the architectural basis of cellular mechanotransduction. Annu. Rev. Physiol. 1997; 59:575-599.
- Ingber DE. Cellular mechanotransduction: putting all the pieces together again. FASEB J. 2006 20: 811-827
- Khalid S. Salaita lab at Emory University
- mechanobio.info (MBInfo)
- Donald Ingber at the Wyss Institute for Biologically Inspired Engineering at Harvard University
- Donald Ingber lab at Children’s Hospital Boston
- Manuela T. Raimondi at Politecnico di Milano
- Michael P. Sheetz at Columbia University
- Martin A. Schwartz at Yale University
- Benjamin Geiger lab at the Weitzmann Institute
- Ning Wang at University of Illinois at Urbana-Champaign
- Christopher S. Chen lab at University of Pennsylvania
- Dennis Discher lab at University of Pennsylvania
- Paul Janmey lab at University of Pennsylvania
- Roger D. Kamm, Massachusetts Institute of Technology
- Ellen Kuhl, Stanford University
- Mechanobiology Lab at University of Pittsburgh School of Medicine
- Cellular Mechanobiology Lab at Penn State
- Charles H. Turner at Indiana University
- Mechanobiology Institute (MBI)
- Merryman Mechanobiology Lab at Vanderbilt University
- Paul Watton, University of Sheffield
- Cecile M Perrault, University of Sheffield
- Ulrich Schwarz, Heidelberg University
- Chaudhuri Lab, Stanford University