Microtubules are hollow cylinders  that are approximately 25nm in diameter  and vary in length from 200 nm to 25 μm. They are formed by the lateral association of between 12 and 17 protofilaments into a regular helical lattice ,. Each protofilament consists of repeating units of polymerized alpha (α) and beta (β) tubulin monomers, all pointed in the same direction. Multiple contacts within the microtubule, between both tubulin subunits and the protofilaments, impart rigidity .
Microtubules are among the stiffest structural elements found in animal cells. Despite this they are often bent by the strong internal forces of the cytoskeleton  and display a resilience to shear and twist forces . This resilience is attributed to protofilament architecture, with internal mechanics providing slack against potentially harmful forces. For example protofilaments have been shown to slide over each other when thermal forces are applied to the microtubule , and can twist along the microtubule axis to provide slack for stretched inter-protofilament bonds .
There are 4 main functions of microtubules:
2. To form the spindle apparatus and ensure the proper segregation of duplicated chromosomes into daughter cells during cell division (i.e. cytokinesis). The spindle apparatus also regulates the assembly and location of the actin-rich contractile ring that pinches and separates the two daughter cells.
3.To form an internal transport network for the trafficking of vesicles containing essential materials to the rest of the cell. This trafficking is mediated by microtubule associated proteins (MAPs) with motor protein activity such as kinesin and dynein.
4. To form a rigid internal core that is used by microtubule-associated motor proteins to generate force and movement in motile structures such as cilia and flagella. A core of microtubules in the neural growth cone and axon also imparts stability and drives neural navigation and guidance.
Microtubules exist in all cells, however their influence in the mechanotransduction of mechanical stimuli has been described at length in cardiac striated muscle  and as such these findings are summarised here:
Mechanical stimuli also affect microtubule formation and proliferation. This has been observed where passive stretching of cardiac muscle was shown to directly affect microtubule formation. In this case, tubulin mRNA and protein levels were shown to be upregulated in response to the passive stretching of neonatal cardiac myocytes . These results were supported by findings of increased proliferation of microtubules following centrifugal force stretch of ventricular myocytes isolated from neonatal rats .
Microtubule proliferation has also been shown to increase the intracellular viscosity of myoctyes and impede sarcomere shortening, which is required to maintain contractility of the cardiac muscle . Changes to these viscoelasticitic properties have been demonstrated in a number of in vitro experiments where physical stresses or the use of agents that selectively disrupt or promote microtubule formation, are applied to cells. In one such case, hypertensive ventricular myocytes were found to be stiffer and more viscous than normotensive ventricular myocytes, a property that was was removed following treatment with colchicine (an inhibitor of microtubule formation) .
It has been well established that myocardial pressure overloading, which results from ventricular hypertrophy, is associated with the loss of cardiac contractility in patients with heart failure . Cooper et al attributed this to an increase in the density of microtubules within cardiac myocytes, where a viscous load is placed on the myofilaments and subsequently impedes sarcomere shortening. In support of their hypothesis, it was shown that treatment with microtubule depolymerizing agents such as colchicine increased contractility .
It has also been reported that mechanotransduction of mechanical stimuli through the microtubule network affects the electrical activity of the heart . This remains controversial however, with different studies reporting opposing findings depending on the model used. For example whilst colchicine treatment (and subsequent microtubule depolymerization) was found to promote arrhythmias in a swine model , it had no effect in rabbits .