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Cardiovascular system hypertrophy

In the cardiovascular system, leptin has been demonstrated to activate components of the MAPK pathways. In cultured neonatal myocytes, ERK1/2 and p38, but not JNK, were activated by leptin inhibiting ERK had no effect, while inhibition of p38 completely inhibited leptin-induced cardiomyocyte hypertrophy (Rajapurohitam et al. 2003). Leptin has also been shown to induce hyperplasia in the immortalized atrial HL-1 cell line via an ERK-dependent pathway (Tajmir et al. [Pg.387]

Cardiovascular system A review discusses chloroquine cardiomyopathy [13 ]. Although a rare occurrence, cardiac toxicity includes conduction disturbances (bxmdle-branch block, atrioventricular block) and cardiomyopathy with hypertrophy, restrictive physiology and congestive heart failure. The review recommends diagnostic procedures. [Pg.394]

Overall, this volume provides a detailed analysis of a wide range of signal transduction systems that mediate hypertrophy, intimal hyperplasia, oxidative damage, contractility, cardiovascular protection, and remodeling. Many components of these signaling pathways are potential targets to develop new therapeutics to treat cardiovascular disorders. [Pg.431]

Patients with CKD are at increased risk of cardiovascular disease, independent of the etiology of their kidney disease. While a clearly unique pathogenesis of cardiovascular disease specific to CKD has not been identified, it is known that manifestations of kidney disease are contributory. Risk factors for cardiovascular disease in this population include hemodynamic and metabolic abnormalities, as well as hypertension, dyslipidemia, elevated homocysteine levels, anemia, hyperparathyroidism, malnutrition, and oxidative stress. Hypertension induced by volume expansion and increased systemic vascular resistance increases myocardial work and contributes to development of left ventricular hypertrophy (LVH). Hyperlipidemia may enhance atherogenesis, while some uremic toxins can decrease myocardial contractflity. In addition, uremic toxins can induce pericarditis, a potentially fatal complication. Currently, measures to screen this high-risk population for cardiovascular risk factors are not routine. ... [Pg.823]

Experiments in animals have found that proliferation of vascular smooth muscle cells can be inhibited by calcitriol administration (Mitsuhashi et al. 1991). An over-active renin-angiotensin system (RAS) can impair renal function and deteriorate cardiovascular health (Li 2012), and down-regulation of RAS activity is one of the key mechanisms proposed for calcitriol (Li et al. 2002). Evidence to support this mechanism has been primarily obtained from animal experiments for example, treatment with calcitriol has been shown to down-regulate RAS and to improve cardiac function in la-hydroxylase knockout mice (Zhou et al. 2008), and in salt-sensitive rats with cardiac hypertrophy (Bae et al. 2011, Choi et al. 2011). However, a recent randomized controlled trial in patients with chronic kidney disease did not find improvements in left ventricular mass index or diastolic function by treatment with paricalcitol (active vitamin D analogue) (Thadhani et al. 2012). [Pg.114]


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Cardiovascular hypertrophy

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