Abstract
The ability of the cells to sense mechanical cues is an integral component of ”social” cell behavior inside tissues with a complex architecture. Through ”mechanosensation” cells are in fact able to decrypt motion, geometries and physical information of surrounding cells and extracellular matrices by activating intracellular pathways converging onto gene expression circuitries controlling cell and tissue homeostasis. Additionally, only recently cell mechanosensation has been integrated systematically as a crucial element in tissue pathophysiology. In the present review, we highlight some of the current efforts to assess the relevance of mechanical sensing into pathology modeling and manufacturing criteria for a next generation of cardiovascular tissue implants.
Highlights
Pathologic evolution of the cardiovascular system is accompanied by modifications in cellular metabolism, aging, epigenetics and risk condition-associated defects and by fundamental changes in cells/tissues architecture, motion and geometry
Apart from neo-vascularization observed in consequence of local activation or repair mechanisms, the cardiovascular system is not endowed with extensive regeneration ability
Evidence of the existence of a mechanical control of cardiac fibroblasts behavior can open new paths in the development of more efficient therapeutic strategies restoring the normal mechanosensing of CFs, taking in consideration inflammatory and metabolic cues
Summary
Pathologic evolution of the cardiovascular system is accompanied by modifications in cellular metabolism, aging, epigenetics and risk condition-associated defects and by fundamental changes in cells/tissues architecture, motion and geometry. The chronic setting of ischemic disease in the heart results in variations in the physical–chemical characteristics of the extracellular matrix, which lead to changes in the structure of the myocytes contractile apparatus (the sarcomere) causing, alternatively, systolic or diastolic heart failure [1] Another example is represented by the chronic alterations of the extracellular matrix in the cardiac valves, where the inflammatory condition consequent to lipid accumulation primes the interstitial cells to acquire a matrix pro-remodeling phenotype, causing tissue calcification [2] and changes in mechanical compliance [3]. A typical example is the adult myocardial tissue, where the presence of cardiogenic cells able to replenish the contractile cells after injury has been dismissed after tense discussions lasting for about two decades [4] This has created a lot of disappointment concerning the feasibility of regenerating the heart to prevent the consequences of heart failure. We discuss aspects of the mechanical-dependent pathological programming of cardiovascular cells to come up with a revision of the current strategies to contextualize physiologic tissue mechanics in cardiovascular tissue engineering procedures
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