Associazione Nazionale Medici Cardiologi Ospedalieri



Heart disease in microgravity: the role of microgravity in metabolic processes in myocardiocytes

Giacinto Omar Roma(Roma) РFondazione Policlinico Campus Bio Medico | Luisini Mario Roma(Roma) РFondazione Policlinico Campus Bio Medico | Sammartini Emanuele Catanzaro(Catanzaro) РUniversità degli studi di Catanzaro Magna Graecia

Objective: Aim of this review is to examine the main molecular patterns alterations during and after exposure to microgravity and find a common molecular stream that may describe the aetiological processes that lead to atrophy of the heart.

Methods: we found 113 articles, and we included 25 studies that investigated physiological effects of weightlessness and artificial gravity in the space flight in animal cardiac muscle cells, in particular the modifications of the protein structure in the absence of gravity.

Result: Microgravity, through methylation on CpG island of the DNA reduces the gene expression of alpha-actinin-1, DNA methyltransferase-1. These molecular values were normal after 12 hours of microgravity suspension, while Histone deacetylase-1 (HDCA-1) resulted up regulated. With regard to cardiogenesis, we noted a reduction in fibronectin, an extracellular matrix glycoprotein that has a role in primordial heart formation to lead to mesodermal migration and differentiation, and in desmosomes which have a particular role in chemical communication between myofibrils; furthermore, an altered displacement of the myofibrils, an alteration of the geometry of these structures and a consequent reduction in cardiac mechanics were noted.Microgravity determines a downregulation of the AC/ cyclic adenosine monophosphate (cAMP) phosphodiesterase system and a secondary dysfunction of the Ca2+ channel; an increase in the levels of the protein Calpain -2 as contributing stressor to myocardial damage is considered an atrophy predisposing risk factor; this protein determines an increase calcium ions and a consequent cardiac remodeling, depression of the ejection fraction and apoptosis of cardiac cells.Another pathological molecular mechanism that leads to alteration of myocardial fibers inotropism is a shift of alpha- Myosin heavy chain to beta- Myosin heavy chain and consequent synthesis of altered titin molecules and a depressed actin/myosin ATPase function.

Conclusion: this review showed molecular patterns role in determining a low performance of the heart caused by a reduction on eject fraction and cardiac atrophy especially after long space flight, due to Microgravity as main risk factor. Future studies are needed to find farmacological and/or molecular approaches to treat these biochemical changes in order to interrupt the chain that leads to a flight and post flight cardiovascular syndromes.