Cellular hypertrophy

Zafeiridis A, Jeevanandam V, Houser SR, Margulies KB. Regression of cellular hypertrophy after left ventricular assist device support. Circulation 1998 98 656-662... 

Fig. 6.3 Proposed model for the Gq-dependent and 3-arrestin2-dependent pathways of ERK1/2 activation. In the Gq-dependent pathway, ERK1/2 translocates to the nucleus while activation of ERK1/2 by the 3-arrestin2 scaffold leads to the sequestration of active ERK1/2 in the cytoplasm, where it activates RSK (see Figure 6.2). The proposed scheme maintains that the Gq-dependent pathway leads to cellular hypertrophy while cytosolic ERK1/2 promotes cell proliferation.

Peroxisome proliferation is consistently associated with hepatomegaly, which arises from a combination of cellular hypertrophy and hyperplasia. Studies on fine structure of hepatocytes revealed that the increase in hepatocyte size was associated with the predominant increase in peroxisomes and modest increase in smooth endoplasmic reticulum (SER). Rats exposed to peroxisome proliferators exhibit 7- to 10-fold increases in peroxisomal relative volume and surface area as evidenced by morphometric analysis of liver sections. The increase in peroxisomal relative volume is due to the increases in both volume and number of peroxisomes. In contrast, the increase in SER surface area and volume rarely exceeds twofold. The magnitude of increase in cellular DNA and... 

The mammalian target of rapamycin complex 1 (mTORCl) system as it is affected by increased nutrients (f AA). The increased AA may interact with the tuberous sclerosis complex 1 or 2 (TSC1 or TSC2), which inhibit Ras homologue enriched in brain (Rheb). The increased AA may also act on Rheb or mTOR directly. Rapamycin inhibits mTOR in this complex, which includes Raptor and the G protein, GpL, which binds to the kinase domain of mTOR both facilitate mTOR signaling. Output from the Raptor protein in mTORCl includes the activation of the ribosomal subunit, S6K, and inhibition of the 4E-binding protein (4E-BP), both of which lead to protein synthesis and cellular hypertrophy. mTOR directly stimulates ribosome synthesis and inhibits autophagy. Arrows indicate stimulatory effects, T-bars indicate inhibition... 

Systolic contractile dysfunction is a cardinal feature of dilated cardiomyopathies. Although the cause of reduced contractility frequently is unknown, abnormalities such as interstitial fibrosis, cellular infiltrates, cellular hypertrophy, and myocardial cell degeneration are seen commonly on histologic examination. ... 

DNA synthesis after 7 weeks. Hence, our results demonstrate a reproducible temporal pattern of early cardiomyocyte ceU proliferation, ceU-cycle withdrawal, and cellular hypertrophy and maturation [54]. 

ARBs potently and selectively inhibit most of the biological effects of Angll, including Angll-induced (1) contraction of vascular smooth muscle, (2) rapid pressor responses, (3) slow pressor responses, (4) thirst, (5) vasopressin release, (6) aldosterone secretion, (7) release of adrenal catecholamines, (8) enhancement of noradrenergic neurotransmission, (9) increases in sympathetic tone, (10) changes in renal function, and (11) cellular hypertrophy and hyperplasia. 

Owens GK, Geisterfer AA, Yang YW, Komoriya A (1988) Transforming growth factor- beta-induced growth inhibition and cellular hypertrophy in cultured vascular smooth muscle cells. J Cell Biol 107 771-780... 

The underlying pathophysiological concepts of treatment by iodine and levothyroxine are different. Iodine aims to reduce cell proliferation and hyperplasia of thy-rocytes, which are regulated by iodine-dependent local growth factors rather than by pituitary-derived TSH. Levothyroxine puts the thyroid to rest by suppressing TSH and reduces cellular hypertrophy due to TSH stimulation (Stubner et al., 1987). A combination of these two agents would therefore, at least in theory, yield additive effects. 

Because the renin-angiotensin pathway is central to the maintenance of blood volume, arterial blood pressure, and electrolyte balance, abnormalities in this pathway (e.g., excessive release of renin and overproduction of angiotensin II) can contribute to a variety of cardiovascular disorders. Specifically, overactivity of this pathway can result in hypertension or heart failure via the mechanisms previously described. Abnormally high levels of angiotensin II can contribute to hypertension through both rapid and slow pressor responses. Additionally, high levels of angiotensin II can cause cellular hypertrophy and increase both afterload and wall tension. All of these events can cause or exacerbate heart failure. 

In mice and rats fed a corn oil extract of kava at doses to 2 g/kg daily for 11 days, abnormal breathing, ataxia, and lethargy were observed. Hepatic cellular hypertrophy was noted in some animals (Sparrow et al. 2004). 

Cellular hypertrophy characterized by calcineurin-NFAT activation and upregulation of hypertrophic transcription factors. Dysregulation of Ca cycling manifesting as contractile arrhythmia... 

The changes in cell kinetic parameters induced in hairless mice by etretinate (1-10 mg/kg/day) were dose-dependent and consisted of transitory cellular hypertrophy, persistent epidermal hyperplasia, and increased labeling indices. The... 

A late effect of the growth promoting action of hormones is the enhancement of DNA synthesis, which is followed by an increase in the number of mitoses. Normally induced growth involves not only cellular hypertrophy, but also tissue hyperplasia. 

After injury, astrocytes undergo a series of morphological and functional alterations termed reactive astro-cytosis, which is characterized by cellular hypertrophy... 

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