1-(5-isoquinolinesulfonyl)-2-methylpiperazine has been researched along with Cardiac Hypertrophy in 16 studies
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine: A specific protein kinase C inhibitor, which inhibits superoxide release from human neutrophils (PMN) stimulated with phorbol myristate acetate or synthetic diacylglycerol.
1-(5-isoquinolinesulfonyl)-2-methylpiperazine : A member of the class of N-sulfonylpiperazines that is 2-methylpiperazine substituted at position 1 by a 5-isoquinolinesulfonyl group.
Cardiac Hypertrophy: Enlargement of the HEART due to chamber HYPERTROPHY, an increase in wall thickness without an increase in the number of cells (MYOCYTES, CARDIAC). It is the result of increase in myocyte size, mitochondrial and myofibrillar mass, as well as changes in extracellular matrix.
Excerpt | Relevance | Reference |
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"Recent evidence indicates that the GTPase activated Rho/Rho-kinase pathway contributes angiotensin II-induced cardiac hypertrophy and vascular remodeling." | 7.73 | Inhibition of Rho-kinase by fasudil attenuated angiotensin II-induced cardiac hypertrophy in apolipoprotein E deficient mice. ( Choy, DF; da Cunha, V; Dole, WP; Halks-Miller, M; Johns, A; Li, W; Light, DR; Mahmoudi, M; Martin-McNulty, B; Schroeder, M; Vincelette, J; Wang, YX, 2005) |
"In this study, the role of the RhoA/Rho-kinase (RhoA/ROCK)-signaling pathway in cardiovascular dysfunction associated with hyperthyroidism was examined with the use of fasudil, a Rho-kinase inhibitor." | 3.78 | RhoA/ROCK may involve in cardiac hypertrophy induced by experimental hyperthyroidism. ( Jianping, Z; Li, C; Na, W; Peng, G; Shengjiang, G; Yanzhong, C, 2012) |
"Recent evidence indicates that the GTPase activated Rho/Rho-kinase pathway contributes angiotensin II-induced cardiac hypertrophy and vascular remodeling." | 3.73 | Inhibition of Rho-kinase by fasudil attenuated angiotensin II-induced cardiac hypertrophy in apolipoprotein E deficient mice. ( Choy, DF; da Cunha, V; Dole, WP; Halks-Miller, M; Johns, A; Li, W; Light, DR; Mahmoudi, M; Martin-McNulty, B; Schroeder, M; Vincelette, J; Wang, YX, 2005) |
"The present study was undertaken to investigate the effect of fasudil, a specific Rho-kinase inhibitor, in pathological cardiac hypertrophy induced by partial abdominal aortic constriction (PAAC) for 4 weeks in comparison with physiological cardiac hypertrophy caused by chronic swimming training (CST) for 8 weeks in rats." | 3.73 | Differential role of rho-kinase in pathological and physiological cardiac hypertrophy in rats. ( Balakumar, P; Singh, M, 2006) |
"Endothelin-1 (ET-1) induces cardiac hypertrophy." | 3.70 | Ca2+/calmodulin-dependent kinase II and calcineurin play critical roles in endothelin-1-induced cardiomyocyte hypertrophy. ( Aikawa, R; Hayashi, D; Komuro, I; Kudoh, S; Mizukami, M; Nagai, R; Shibasaki, F; Shiojima, I; Toko, H; Yazaki, Y; Zhu, W; Zou, Y, 2000) |
"Hypertensive cardiac hypertrophy is associated with reduced coronary flow reserve, but its impact on coronary flow regulation and vasomotor function remains incompletely understood and requires further investigation." | 1.46 | Enhanced endothelin-1/Rho-kinase signalling and coronary microvascular dysfunction in hypertensive myocardial hypertrophy. ( Hein, TW; Kuo, L; Lu, G; Ren, Y; Tsai, SH; Xu, X, 2017) |
"Pathologic cardiac hypertrophy is one of the leading causes of sudden death from cardiac disease and involves a complex network of bio-signaling mechanisms." | 1.42 | N-[(11)C]-methyl-hydroxyfasudil is a potential biomarker of cardiac hypertrophy. ( DaSilva, JN; Fernando, P; Moreau, S; Valdivia, A, 2015) |
Timeframe | Studies, this research(%) | All Research% |
---|---|---|
pre-1990 | 0 (0.00) | 18.7374 |
1990's | 1 (6.25) | 18.2507 |
2000's | 6 (37.50) | 29.6817 |
2010's | 9 (56.25) | 24.3611 |
2020's | 0 (0.00) | 2.80 |
Authors | Studies |
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Tsai, SH | 1 |
Lu, G | 1 |
Xu, X | 2 |
Ren, Y | 1 |
Hein, TW | 1 |
Kuo, L | 1 |
Zhuang, R | 1 |
Wu, J | 1 |
Lin, F | 1 |
Han, L | 1 |
Liang, X | 1 |
Meng, Q | 1 |
Jiang, Y | 1 |
Wang, Z | 1 |
Yue, A | 1 |
Gu, Y | 1 |
Fan, H | 1 |
Zhou, X | 1 |
Liu, Z | 1 |
Ocaranza, MP | 1 |
Fierro, C | 1 |
Jalil, JE | 1 |
Moya, J | 1 |
Gonzalez, L | 1 |
Molina, C | 1 |
Mancilla, C | 1 |
Yan, X | 1 |
Jiao, K | 1 |
Song, X | 1 |
Moreau, S | 1 |
DaSilva, JN | 1 |
Valdivia, A | 1 |
Fernando, P | 1 |
Ying, Z | 1 |
Yue, P | 1 |
Zhong, M | 1 |
Sun, Q | 1 |
Mikolaj, M | 1 |
Wang, A | 1 |
Brook, RD | 1 |
Chen, LC | 1 |
Rajagopalan, S | 1 |
Na, W | 1 |
Peng, G | 1 |
Jianping, Z | 1 |
Yanzhong, C | 1 |
Shengjiang, G | 1 |
Li, C | 1 |
Ho, TJ | 1 |
Huang, CC | 1 |
Huang, CY | 1 |
Lin, WT | 1 |
Satoh, S | 1 |
Kawasaki, K | 1 |
Ikegaki, I | 1 |
Asano, T | 1 |
Shimokawa, H | 2 |
Zhang, ZJ | 1 |
Fan, YF | 1 |
Zhang, ZY | 1 |
Xie, PY | 1 |
Fang, HC | 1 |
Su, YS | 1 |
Higashi, M | 1 |
Hattori, T | 1 |
Hiroki, J | 1 |
Mukai, Y | 1 |
Morikawa, K | 1 |
Ichiki, T | 1 |
Takahashi, S | 1 |
Takeshita, A | 1 |
Wang, YX | 1 |
da Cunha, V | 1 |
Martin-McNulty, B | 1 |
Vincelette, J | 1 |
Li, W | 1 |
Choy, DF | 1 |
Halks-Miller, M | 1 |
Mahmoudi, M | 1 |
Schroeder, M | 1 |
Johns, A | 1 |
Light, DR | 1 |
Dole, WP | 1 |
Balakumar, P | 1 |
Singh, M | 1 |
McKinsey, TA | 1 |
Kass, DA | 1 |
Murata, M | 1 |
Fukuda, K | 1 |
Ishida, H | 1 |
Miyoshi, S | 1 |
Koura, T | 1 |
Kodama, H | 1 |
Nakazawa, HK | 1 |
Ogawa, S | 1 |
Zhu, W | 1 |
Zou, Y | 1 |
Shiojima, I | 1 |
Kudoh, S | 1 |
Aikawa, R | 1 |
Hayashi, D | 1 |
Mizukami, M | 1 |
Toko, H | 1 |
Shibasaki, F | 1 |
Yazaki, Y | 1 |
Nagai, R | 1 |
Komuro, I | 1 |
1 review available for 1-(5-isoquinolinesulfonyl)-2-methylpiperazine and Cardiac Hypertrophy
Article | Year |
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Small-molecule therapies for cardiac hypertrophy: moving beneath the cell surface.
Topics: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; Amides; Animals; Cardiomegaly; Cardiovascular Agents; | 2007 |
15 other studies available for 1-(5-isoquinolinesulfonyl)-2-methylpiperazine and Cardiac Hypertrophy
Article | Year |
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Enhanced endothelin-1/Rho-kinase signalling and coronary microvascular dysfunction in hypertensive myocardial hypertrophy.
Topics: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; Animals; Arterioles; Cardiomegaly; Endothelin-1; Endo | 2017 |
Fasudil preserves lung endothelial function and reduces pulmonary vascular remodeling in a rat model of end‑stage pulmonary hypertension with left heart disease.
Topics: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; Animals; Cardiomegaly; Cell Line; Heart Diseases; Hum | 2018 |
Rho kinase activation in circulating leukocytes is related to hypertensive myocardial remodeling.
Topics: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; Animals; Atrial Remodeling; Blood Pressure; Cardiomeg | 2018 |
Shen'ge powder decreases the cardiomyocyte hypertrophy in chronic heart failure by activating the Rho protein/Rho-associated coiledcoil forming protein kinase signaling pathway.
Topics: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; Animals; Apoptosis; Cardiomegaly; Cell Survival; Dise | 2019 |
N-[(11)C]-methyl-hydroxyfasudil is a potential biomarker of cardiac hypertrophy.
Topics: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; Animals; Biomarkers; Cardiomegaly; Cell Nucleus; Cell | 2015 |
Air pollution and cardiac remodeling: a role for RhoA/Rho-kinase.
Topics: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; Angiotensin II; Animals; Atmosphere Exposure Chambers | 2009 |
RhoA/ROCK may involve in cardiac hypertrophy induced by experimental hyperthyroidism.
Topics: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; Animals; Apoptosis; bcl-2-Associated X Protein; Cardi | 2012 |
Fasudil, a Rho-kinase inhibitor, protects against excessive endurance exercise training-induced cardiac hypertrophy, apoptosis and fibrosis in rats.
Topics: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; Animals; Apoptosis; Apoptosis Regulatory Proteins; Bi | 2012 |
Evidence of a direct cellular protective effect of Rho-kinase inhibitors on endothelin-induced cardiac myocyte hypertrophy.
Topics: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; Animals; Cardiomegaly; Cells, Cultured; Cytoprotectio | 2012 |
[Effects of rho-kinase inhibitor on cardiac hypertrophy of left ventricle in spontaneously hypertensive rats].
Topics: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; Animals; Cardiomegaly; Heart Ventricles; Male; Nifedi | 2012 |
Long-term inhibition of Rho-kinase suppresses angiotensin II-induced cardiovascular hypertrophy in rats in vivo: effect on endothelial NAD(P)H oxidase system.
Topics: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; Angiotensin II; Animals; Aorta, Thoracic; Cardiomegal | 2003 |
Inhibition of Rho-kinase by fasudil attenuated angiotensin II-induced cardiac hypertrophy in apolipoprotein E deficient mice.
Topics: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; Angiotensin II; Animals; Apolipoproteins E; Atrial Na | 2005 |
Differential role of rho-kinase in pathological and physiological cardiac hypertrophy in rats.
Topics: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; Adaptation, Physiological; Animals; Blood Pressure; C | 2006 |
Leukemia inhibitory factor, a potent cardiac hypertrophic cytokine, enhances L-type Ca2+ current and [Ca2+]i transient in cardiomyocytes.
Topics: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; Animals; Calcium; Calcium-Calmodulin-Dependent Protei | 1999 |
Ca2+/calmodulin-dependent kinase II and calcineurin play critical roles in endothelin-1-induced cardiomyocyte hypertrophy.
Topics: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; Animals; Animals, Newborn; Calcimycin; Calcineurin; C | 2000 |