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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Myocardial fibrosis &#8211; perivascular&#44; interstitial or replacement &#40;scar&#41;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> &#8211; is the endpoint of various pathological settings&#44; often leading to dismal outcomes&#44; including heart failure&#44; arrhythmias and sudden death&#46; In hypertensive heart disease&#44; patterns of perivascular and interstitial myocardial fibrosis are common and may easily be shown and graded&#44; in formalin-fixed samples&#44; with histochemical stains such as Masson trichrome&#44; elastic Van Gieson&#44; or picrosirius red&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">Experimental and human studies<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> have demonstrated that myocardial fibrosis is the result of various promoters&#44; among which are mast cells&#46;<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">3&#8211;10</span></a> Discovered and named by the Nobel prize-winning German physician Paul Ehrlich in 1878&#44;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">3</span></a> mast cells are immune cells derived from bone marrow precursors and resident in tissues&#46; They are usually classified as typical if located in connective tissue such as the myocardium&#44; or atypical if located elsewhere&#44; and as MCT if their granules contain tryptase&#44; MCC if they contain chymase or MCTC if they contain both proteases&#46;<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">3&#44;4</span></a> Anti-chymase or anti-tryptase antibodies are used for immunohistochemical identification of mast cells in situ&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">9</span></a> Mast cells are also known have a wide range of mediators &#40;histamine&#44; cytokines&#44; growth factors and vasoactive agents&#41; that affect tissue remodeling as pro- or anti-fibrotic agents&#46;<a class="elsevierStyleCrossRefs" href="#bib0070"><span class="elsevierStyleSup">4&#8211;7</span></a> The effect of cardiac mast cells on myocardial fibrosis may result both from degranulation and from de novo secretion of mediators common to other cells&#44; including tumor necrosis factor alpha and beta&#44; interleukin 4 and platelet-derived growth factor&#44; as well as from the roles of chymase and&#47;or tryptase&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> The fibrogenic action of chymase may follow two pathways&#58; the formation of angiotensin II through activation of the angiotensin-converting enzyme-independent chymase pathway&#44; and activation of matrix metalloproteinases&#46;<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">1&#44;4&#44;7</span></a> Tryptase activates fibroblast proliferation and collagen I synthesis&#44; mainly by activating protease-activated receptor-2&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">There is controversy concerning the pro-fibrotic and anti-fibrotic phenotypes of mast cells&#58; whether the phenotypes can switch depending on the environment and genetics&#44; and whether fibrotic tissue can regress as a consequence of a switch to the anti-fibrotic version&#59; what are the key points of therapeutic intervention&#59; and other questions&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">Some authors point out limitations in research into human cardiac fibrosis and its relation to mast cells&#44; due both to the characteristics of the samples used&#44; whether obtained from biopsy or autopsy&#44; and to the difficulty in obtaining normal control tissue&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">7</span></a> Myocardial biopsies are limited in their size and location&#44; although if morphological alterations are identified and appropriate complementary techniques are applied&#44; useful data may be obtained&#46; Furthermore&#44; despite the difficulties in preserving autopsy material&#44; if basic preservative measures are routinely applied&#44; it may provide large quantities of disease samples and normal controls&#44; as exemplified by the study by Juliano et al&#46; published in this issue of the <span class="elsevierStyleItalic">Journal</span>&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">9</span></a></p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0025" class="elsevierStylePara elsevierViewall">The author has no conflicts of interest to declare&#46;</p></span></span>"
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Editorial comment
Mast cells: Promoters of myocardial fibrosis in hypertensive heart disease?
Mastócitos: promotores da fibrose miocárdica na doença hipertensiva cardíaca?
Rosa Henriques de Gouveia
Pathological Anatomy, Instituto Nacional de Medicina Legal e Ciências Forenses, Coimbra, Portugal
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        "titulo" => "Mast&#243;citos&#58; promotores da fibrose mioc&#225;rdica na doen&#231;a hipertensiva card&#237;aca&#63;"
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Myocardial fibrosis &#8211; perivascular&#44; interstitial or replacement &#40;scar&#41;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> &#8211; is the endpoint of various pathological settings&#44; often leading to dismal outcomes&#44; including heart failure&#44; arrhythmias and sudden death&#46; In hypertensive heart disease&#44; patterns of perivascular and interstitial myocardial fibrosis are common and may easily be shown and graded&#44; in formalin-fixed samples&#44; with histochemical stains such as Masson trichrome&#44; elastic Van Gieson&#44; or picrosirius red&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">Experimental and human studies<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> have demonstrated that myocardial fibrosis is the result of various promoters&#44; among which are mast cells&#46;<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">3&#8211;10</span></a> Discovered and named by the Nobel prize-winning German physician Paul Ehrlich in 1878&#44;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">3</span></a> mast cells are immune cells derived from bone marrow precursors and resident in tissues&#46; They are usually classified as typical if located in connective tissue such as the myocardium&#44; or atypical if located elsewhere&#44; and as MCT if their granules contain tryptase&#44; MCC if they contain chymase or MCTC if they contain both proteases&#46;<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">3&#44;4</span></a> Anti-chymase or anti-tryptase antibodies are used for immunohistochemical identification of mast cells in situ&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">9</span></a> Mast cells are also known have a wide range of mediators &#40;histamine&#44; cytokines&#44; growth factors and vasoactive agents&#41; that affect tissue remodeling as pro- or anti-fibrotic agents&#46;<a class="elsevierStyleCrossRefs" href="#bib0070"><span class="elsevierStyleSup">4&#8211;7</span></a> The effect of cardiac mast cells on myocardial fibrosis may result both from degranulation and from de novo secretion of mediators common to other cells&#44; including tumor necrosis factor alpha and beta&#44; interleukin 4 and platelet-derived growth factor&#44; as well as from the roles of chymase and&#47;or tryptase&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> The fibrogenic action of chymase may follow two pathways&#58; the formation of angiotensin II through activation of the angiotensin-converting enzyme-independent chymase pathway&#44; and activation of matrix metalloproteinases&#46;<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">1&#44;4&#44;7</span></a> Tryptase activates fibroblast proliferation and collagen I synthesis&#44; mainly by activating protease-activated receptor-2&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">There is controversy concerning the pro-fibrotic and anti-fibrotic phenotypes of mast cells&#58; whether the phenotypes can switch depending on the environment and genetics&#44; and whether fibrotic tissue can regress as a consequence of a switch to the anti-fibrotic version&#59; what are the key points of therapeutic intervention&#59; and other questions&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">Some authors point out limitations in research into human cardiac fibrosis and its relation to mast cells&#44; due both to the characteristics of the samples used&#44; whether obtained from biopsy or autopsy&#44; and to the difficulty in obtaining normal control tissue&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">7</span></a> Myocardial biopsies are limited in their size and location&#44; although if morphological alterations are identified and appropriate complementary techniques are applied&#44; useful data may be obtained&#46; Furthermore&#44; despite the difficulties in preserving autopsy material&#44; if basic preservative measures are routinely applied&#44; it may provide large quantities of disease samples and normal controls&#44; as exemplified by the study by Juliano et al&#46; published in this issue of the <span class="elsevierStyleItalic">Journal</span>&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">9</span></a></p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0025" class="elsevierStylePara elsevierViewall">The author has no conflicts of interest to declare&#46;</p></span></span>"
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ISSN: 21742049
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Revista Portuguesa de Cardiologia (English edition)
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