Apoptosis inhibition of cellular proliferation by II: possible implication and perspectives

Abstract
The\ud renin-angiotensin\ud system\ud plays\ud a\ud pivotal\ud role\ud in\ud the\ud regulation\ud of\ud fluid,\ud electrolyte\ud metabolism\ud and\ud blood\ud pressure.\ud Molecular\ud cloning\ud and\ud pharmacological\ud studies\ud have\ud defined\ud two\ud major\ud classes\ud of\ud Angiotensin\ud II\ud (Ang\ud II)\ud receptors,\ud designated\ud AT1\ud and\ud AT2.\ud Recently,\ud it\ud has\ud been\ud well\ud recognized\ud that\ud Ang\ud II,\ud beside\ud its\ud classical\ud physiological\ud actions,\ud is\ud a\ud profibrogenic\ud peptide\ud and\ud displays\ud characteristics\ud of\ud a\ud growth\ud factor.\ud The\ud emerging\ud picture\ud suggests\ud that\ud angiotensin\ud receptor\ud subtypes\ud exert\ud opposing\ud features\ud in\ud many\ud aspects\ud of\ud their\ud biological\ud function,\ud most\ud importantly\ud in\ud cellular\ud growth\ud and\ud proliferation.\ud Accordingly,\ud the\ud proliferative\ud and/or\ud growth-promoting\ud effects\ud of\ud Ang\ud II\ud are\ud thought\ud to\ud be\ud mediated\ud by\ud AT1\ud receptor,\ud whereas\ud the\ud AT2\ud receptor\ud subtype\ud may\ud have\ud growth-inhibitory\ud properties.\ud The\ud novel\ud finding\ud that\ud Ang\ud II\ud is\ud able\ud to\ud induce\ud apoptosis\ud by\ud AT\ud 2\ud receptors\ud in\ud diverse\ud cell\ud types\ud is\ud of\ud great\ud scientific\ud interest,\ud as\ud recent\ud studies\ud revealed\ud a\ud role\ud for\ud apoptosis\ud as\ud a\ud deliberate\ud form\ud of\ud cell\ud death\ud in\ud the\ud pathogenesis\ud of\ud various\ud cardiovascular\ud diseases\ud such\ud as\ud heart\ud failure\ud and\ud vascular\ud remodeling.\ud Furthermore\ud apoptotic\ud cell\ud death\ud might\ud occur\ud during\ud the\ud development\ud of\ud progressive\ud glomerulosclerosis.\ud It\ud is\ud tempting\ud to\ud speculate\ud that\ud autocrine-paracrine\ud vasoactive\ud substances\ud such\ud as\ud Ang\ud II\ud might\ud regulate\ud these\ud apoptotic\ud processes\ud during\ud pathogenic\ud conditions

This publication has 93 references indexed in Scilit: