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23248151 10.1161/HYPERTENSIONAHA.111.00562 1:CAS:528:DC%2BC3sXhtFymtL4%3D
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Sun B, Huo R, Sheng Y, et al. Bone morphogenetic protein-4 mediates cardiac hypertrophy, apoptosis, and fibrosis in experimentally pathological cardiac hypertrophy. Hypertension. 2013;61:352-60.
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Sun, B.1
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Molecular mechanisms underlying cardiac antihypertrophic and antifibrotic effects of natriuretic peptides
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10.1007/s00109-011-0801-z 1:CAS:528:DC%2BC38Xks1yiuw%3D%3D
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Calvieri C, Rubattu S, Volpe M. Molecular mechanisms underlying cardiac antihypertrophic and antifibrotic effects of natriuretic peptides. J Mol Med (Berl). 2012;90:5-13.
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Lowered B-type natriuretic peptide in response to levosimendan or dobutamine treatment is associated with improved survival in patients with severe acutely decompensated heart failure
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19539144 10.1016/j.jacc.2009.02.058 1:CAS:528:DC%2BD1MXovFShtLo%3D
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Cohen-Solal A, Logeart D, Huang B, et al. Lowered B-type natriuretic peptide in response to levosimendan or dobutamine treatment is associated with improved survival in patients with severe acutely decompensated heart failure. J Am Coll Cardiol. 2009;53:2343-8.
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42
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7244255799
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Atrial natriuretic peptide dose-dependently inhibits pressure overload-induced cardiac remodeling
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15452027 10.1161/01.HYP.0000144801.09557.4c 1:CAS:528: DC%2BD2cXovVCgt70%3D
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Franco V, Chen YF, Oparil S, et al. Atrial natriuretic peptide dose-dependently inhibits pressure overload-induced cardiac remodeling. Hypertension. 2004;44:746-50.
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Franco, V.1
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43
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Atrial natriuretic peptide inhibits transforming growth factor beta-induced Smad signaling and myofibroblast transformation in mouse cardiac fibroblasts
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17991884 10.1161/CIRCRESAHA.107.157677 1:CAS:528:DC%2BD1cXhtVGktL0%3D This paper details the mechanism of the anti-fibrotic action of the atrial natriuretic peptide. BNP acts by the same ways. So, these peptides are not only diuretic, but essential to limit, if possible, the cardiac fibrosis
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•• Li P, Wang D, Lucas J, et al. Atrial natriuretic peptide inhibits transforming growth factor beta-induced Smad signaling and myofibroblast transformation in mouse cardiac fibroblasts. Circ Res. 2008;102:185-92. This paper details the mechanism of the anti-fibrotic action of the atrial natriuretic peptide. BNP acts by the same ways. So, these peptides are not only diuretic, but essential to limit, if possible, the cardiac fibrosis.
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Circ Res
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Li, P.1
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44
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Cardiac fibrosis in mice lacking brain natriuretic peptide
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10737768 10.1073/pnas.070371497 1:CAS:528:DC%2BD3cXislSgu7g%3D
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Tamura N, Ogawa Y, Chusho H, et al. Cardiac fibrosis in mice lacking brain natriuretic peptide. Proc Natl Acad Sci U S A. 2000;97:4239-44.
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Tamura, N.1
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45
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B-type natriuretic peptide attenuates cardiac hypertrophy via the transforming growth factor-ss1/smad7 pathway in vivo and in vitro
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19719752 10.1111/j.1440-1681.2009.05281.x 1:CAS:528:DC%2BC3cXjslemsLk%3D
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He JG, Chen YL, Chen BL, et al. B-type natriuretic peptide attenuates cardiac hypertrophy via the transforming growth factor-ss1/smad7 pathway in vivo and in vitro. Clin Exp Pharmacol Physiol. 2010;37:283-9.
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He, J.G.1
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46
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A genetically clamped renin transgene for the induction of hypertension
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12034874 10.1073/pnas.112222199 1:CAS:528:DC%2BD38XkvVGhtbs%3D
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Caron KM, James LR, Kim HS, et al. A genetically clamped renin transgene for the induction of hypertension. Proc Natl Acad Sci U S A. 2002;99:8248-52.
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Caron, K.M.1
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47
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Restoration of podocyte structure and improvement of chronic renal disease in transgenic mice overexpressing renin
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19696925 10.1371/journal.pone.0006721
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Huby AC, Rastaldi MP, Caron K, et al. Restoration of podocyte structure and improvement of chronic renal disease in transgenic mice overexpressing renin. PLoS One. 2009;4:e6721.
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Huby, A.C.1
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48
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Cardiac specific increase in aldosterone production induces coronary dysfunction in aldosterone synthase-transgenic mice
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15364804 10.1161/01.CIR.0000142858.44680.27 1:CAS:528: DC%2BD2cXnslems70%3D
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Garnier A, Bendall JK, Fuchs S, et al. Cardiac specific increase in aldosterone production induces coronary dysfunction in aldosterone synthase-transgenic mice. Circulation. 2004;110:1819-25.
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Garnier, A.1
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Fuchs, S.3
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49
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57449102566
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Cross-talk between mineralocorticoid and angiotensin II signaling for cardiac remodeling
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18981328 10.1161/HYPERTENSIONAHA.108.117531 1:CAS:528:DC%2BD1cXhsVWrt7vJ
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Di Zhang A, Nguyen Dinh Cat A, Soukaseum C, et al. Cross-talk between mineralocorticoid and angiotensin II signaling for cardiac remodeling. Hypertension. 2008;52:1060-7.
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Di Zhang, A.1
Nguyen Dinh Cat, A.2
Soukaseum, C.3
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50
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79953199333
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The mineralocorticoid receptor in heart: Different effects in different cells
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21321302 10.1161/HYPERTENSIONAHA.110.164962 1:CAS:528: DC%2BC3MXjt1Gnsro%3D
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Jaisser F, Swynghedauw B, Delcayre C. The mineralocorticoid receptor in heart: different effects in different cells. Hypertension. 2011;57:679-80.
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Jaisser, F.1
Swynghedauw, B.2
Delcayre, C.3
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51
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Mineralocorticoid receptor inhibition ameliorates the transition to myocardial failure and decreases oxidative stress and inflammation in mice with chronic pressure overload
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15687129 10.1161/01.CIR.0000153800.09920.40 1:CAS:528: DC%2BD2MXmvFGhsg%3D%3D
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Kuster GM, Kotlyar E, Rude MK, et al. Mineralocorticoid receptor inhibition ameliorates the transition to myocardial failure and decreases oxidative stress and inflammation in mice with chronic pressure overload. Circulation. 2005;111:420-7.
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Kuster, G.M.1
Kotlyar, E.2
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52
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79953224745
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Ablation of mineralocorticoid receptors in myocytes but not in fibroblasts preserves cardiac function
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21321305 10.1161/HYPERTENSIONAHA.110.163287 1:CAS:528: DC%2BC3MXjt1Gns7g%3D This paper, and the two following ones, took advantage of invalidation of the MR in mice to decipher the role of this receptor in different cell types. The present paper used fibroblast-specific and cardiomyocyte-specific MR KO; it showed that MR in cardiac myocytes, but not in fibroblasts, protect from cardiac dilatation and failure after chronic pressure overload
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• Lother A, Berger S, Gilsbach R, et al. Ablation of mineralocorticoid receptors in myocytes but not in fibroblasts preserves cardiac function. Hypertension. 2011;57:746-54. This paper, and the two following ones, took advantage of invalidation of the MR in mice to decipher the role of this receptor in different cell types. The present paper used fibroblast-specific and cardiomyocyte-specific MR KO; it showed that MR in cardiac myocytes, but not in fibroblasts, protect from cardiac dilatation and failure after chronic pressure overload.
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(2011)
Hypertension
, vol.57
, pp. 746-754
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Lother, A.1
Berger, S.2
Gilsbach, R.3
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53
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70349257487
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Deletion of mineralocorticoid receptors from macrophages protects against deoxycorticosterone/salt-induced cardiac fibrosis and increased blood pressure
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19635989 10.1161/HYPERTENSIONAHA.109.131110 1:CAS:528: DC%2BD1MXpsleksrk%3D This paper used macrophage-specific MR KO to demonstrate for the first time that macrophage recruitment is not altered by loss of MR signaling in these cells, and that a novel and significant role is seen for macrophage signaling in the regulation of cardiac fibrosis in the DOCA/salt model
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•• Rickard AJ, Morgan J, Tesch G, et al. Deletion of mineralocorticoid receptors from macrophages protects against deoxycorticosterone/salt-induced cardiac fibrosis and increased blood pressure. Hypertension. 2009;54:537-43. This paper used macrophage-specific MR KO to demonstrate for the first time that macrophage recruitment is not altered by loss of MR signaling in these cells, and that a novel and significant role is seen for macrophage signaling in the regulation of cardiac fibrosis in the DOCA/salt model.
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(2009)
Hypertension
, vol.54
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Rickard, A.J.1
Morgan, J.2
Tesch, G.3
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54
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77956388193
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Myeloid mineralocorticoid receptor controls macrophage polarization and cardiovascular hypertrophy and remodeling in mice
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20697155 10.1172/JCI41080 1:CAS:528:DC%2BC3cXhtFertbvK This well documented study myeloid cells-specific knockout of the MR gene to show that myeloid MR is critical in controlling the macrophage polarization. Macrophages from myeloid MR KO mice exhibited a transcription profile of alternative activation. In isolated macrophages, pharmacologic MR blockade has similar effects, thus demonstrating that fibrosis depends of direct effects on the macrophages
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• Usher MG, Duan SZ, Ivaschenko CY, et al. Myeloid mineralocorticoid receptor controls macrophage polarization and cardiovascular hypertrophy and remodeling in mice. J Clin Invest. 2010;120:3350-64. This well documented study myeloid cells-specific knockout of the MR gene to show that myeloid MR is critical in controlling the macrophage polarization. Macrophages from myeloid MR KO mice exhibited a transcription profile of alternative activation. In isolated macrophages, pharmacologic MR blockade has similar effects, thus demonstrating that fibrosis depends of direct effects on the macrophages.
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(2010)
J Clin Invest
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Usher, M.G.1
Duan, S.Z.2
Ivaschenko, C.Y.3
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55
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84862737919
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Macrophage mineralocorticoid receptor signaling plays a key role in aldosterone-independent cardiac fibrosis
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22653557 10.1210/en.2011-2098 1:CAS:528:DC%2BC38XpsFWnsrs%3D
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Bienvenu LA, Morgan J, Rickard AJ, et al. Macrophage mineralocorticoid receptor signaling plays a key role in aldosterone-independent cardiac fibrosis. Endocrinology. 2012;153:3416-25.
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Bienvenu, L.A.1
Morgan, J.2
Rickard, A.J.3
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56
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84856347698
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Aldosterone and mineralocorticoid receptors: A personal reflection
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22155566 10.1016/j.mce.2011.11.026 1:CAS:528:DC%2BC38Xhs1CqtLY%3D
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Funder JW. Aldosterone and mineralocorticoid receptors: a personal reflection. Mol Cell Endocrinol. 2012;350:146-50.
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Funder, J.W.1
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57
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84873055223
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Aldosterone-specific activation of cardiomyocyte mineralocorticoid receptor in vivo
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23297371 10.1161/HYPERTENSIONAHA.112.198986 1:CAS:528: DC%2BC3sXhtFymtL8%3D
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Messaoudi S, Gravez B, Tarjus A, et al. Aldosterone-specific activation of cardiomyocyte mineralocorticoid receptor in vivo. Hypertension. 2013;61:361-7.
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Hypertension
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Messaoudi, S.1
Gravez, B.2
Tarjus, A.3
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