
SINALIZAÇÃO INTRACELULAR DE CÉLULAS CONTRÁTEIS EXCITAVEIS MEDIADAS PELO CA2+ NA HOMEOSTASE E NA DOENÇA
2020; Frederico Kauffmann Barbosa; Volume: 17; Issue: 46 Linguagem: Português
ISSN
1807-8850
Autores Tópico(s)Cardiac pacing and defibrillation studies
ResumoIntroducao: O sistema cardiovascular faz com que o sangue circule e transporte oxigenio e nutrientes para o corpo atraves da contracao das celulas cardiacas. Durante este processo, inumeros eventos de sinalizacao intracelular envolvem a participacao do Ca2+. Metodologia: A revisao foi realizada por base de dados bibliograficos obtidos atraves da pesquisa em LILACS, MEDLINE e PubMed. Resultados: A concentracao citoplasmatica basal de Ca2+ e regulada por canais de Ca2+, ATPases, transportadores e proteinas de ligacao do Ca2+. A entrada de Ca2+ promove a liberacao de mais Ca2+ do reticulo sarcoplasmatico por meio dos receptores de rianodina, que se ligam a troponina C causando o movimento da tropomiosina e exposicao do sitio receptor da miosina, permitindo a ligacao com a actina e contracao celular. Para que ocorra o relaxamento celular, o Ca2+ precisa ser removido do citosol por recaptacao pela isoforma cardiaca do reticulo sarcoplasmico Ca2+-ATPase; extrusao pelo canal trocador Na+/Ca2+; acao da Ca2+ ATPase da membrana plasmatica e recaptacao mitocondrial de Ca2+. Alteracoes nestes mecanismos levam a reativacao de genes expressos durante a vida fetal, contribuindo para o processo de hipertrofia cardiaca. Conclusao: A manutencao destes mecanismos de sinalizacao com a participacao do Ca2+ sao fundamentais para a homeostase das celulas cardiacas, e alteracoes neste processo podem levar a sobrecarga funcional e hipertrofia das celulas cardiacas. INTRACELLULAR SIGNALING OF EXCITABLE CONTRACTILE CELLS MEDIATED BY CA2+ IN HOMEOSTASIS AND DISEASE Introduction: The cardiovascular system sends blood and transport oxygen and nutrients to the body through the contraction of cardiac cells. During this process, numerous intracellular signaling events involve the participation of Ca2+. Methodology: The review was carried out using bibliographic databases obtained through research in LILACS, MEDLINE and PubMed. Results: The basal cytoplasmic Ca2+ concentration is regulated by Ca2+ channels, ATPases, transporters and Ca2+ binding proteins. The entry of Ca2+ promotes the release of more Ca2+ from the sarcoplasmic reticulum through the ryanodine receptors, which bind to troponin C causing the movement of tropomyosin and exposure of the myosin receptor site, allowing binding with actin and cell contraction. For cell relaxation to occur, Ca2+ needs to be removed from the cytosol with reuptake by the cardiac isoform of the sarcoplasmic reticulum Ca2+-ATPase; extrusion through the Na+/Ca2+ exchanger channel; action of plasma membrane Ca2+ ATPase and mitochondrial Ca2+ reuptake. Changes in these mechanisms lead to reactivation of genes expressed during fetal life, contributing to the process of cardiac hypertrophy. Conclusion: The maintenance of these signaling mechanisms with the participation of Ca2+ is fundamental for the homeostasis of cardiac cells, and changes in this process can lead to functional overload and hypertrophy of cardiac cells.
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