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What role does intracellular and intercellular signaling play in cardiac remodeling?
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Dialogues in Cardiovascular Medicine
Volume 20, Issue 2, 2015, Pages 107-118
What role does intracellular and intercellular signaling play in cardiac remodeling? (Article)
Rizzo, P.a ,
Ameri, P.b
a Department of Morphology, Surgery, and Experimental Medicine, Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, Ferrara, Italy
b Research Center of Cardiovascular Biology, Department of Internal Medicine, University of Genova, Genova, Italy
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Abstract
Pathological cardiac remodeling leads to progressive worsening of cardiac function and heart failure. Novel and more effective therapeutic strategies are needed to slow down or reverse this often fatal process. The dissection of the molecular events underlying cardiac remodeling could lead to the identification of promising new candidates for targeted treatment of heart failure. In this review, we discuss the role of the Notch and Akt (protein kinase B) signaling pathways in mediating intercellular and intracellular events that play an important role in the myocardium under physiological and pathological conditions, including remodeling
When and how? Two simple questions to determine cancer status and inform therapeutic decisions and trial design in heart failure
No full textDiffuse Endocrine System, Neuroendocrine Tumors and Immunity: What's New?
No full textDuring the last two decades, research into the modulation of immunity by the neuroendocrine system has flourished, unravelling significant effects of several neuropeptides, including somatostatin (SRIH), and especially cortistatin (CST), on immune cells. Scientists have learnt that the diffuse neuroendocrine system can regulate the immune system at all its levels: innate immunity, adaptive immunity, and maintenance of immune tolerance. Compelling studies with animal models have demonstrated that some neuropeptides may be effective in treating inflammatory disorders, such as sepsis, and T helper 1-driven autoimmune diseases, like Crohn's disease and rheumatoid arthritis. Here, the latest findings concerning the neuroendocrine control of the immune system are discussed, with emphasis on SRIH and CST. The second part of the review deals with the immune response to neuroendocrine tumors (NETs). The anti-NET immune response has been described in the last years and it is still being characterized, similarly to what is happening for several other types of cancer. In parallel with investigations addressing the mechanisms by which the immune system contrasts NET growth and spreading, ground-breaking clinical trials of dendritic cell vaccination as immunotherapy for metastatic NETs have shown in principle that the immune reaction to NETs can be exploited for treatment
Pasireotide, an IGF-I action inhibitor, prevents growth hormone and estradiol-induced mammary hyperplasia.
No full textMammary hyperplasia increases breast cancer risk. Tamoxifen prevents breast cancer in women with atypical hyperplasia, but has serious side effects. As estradiol action requires IGF-I, direct inhibition of IGF-I action theoretically might be an efficacious alternative to tamoxifen. After hypophysectomy and oophorectomy, 21-day-old female rats were treated with GH and E2. After 7 days all terminal end buds (TEBs) and 75% of ducts became hyperplastic. Co-treatment with pasireotide, a somatostatin analog that blocks GH secretion and IGF-I action in the mammary gland, prevented hormone-induced hyperplasia. The number and size of TEBs and moderately or floridly hyperplastic ducts was reduced by pasireotide (P < 0.01). In contrast, the same concentration of octreotide, which has a more selective somatostatin receptor subtype binding profile, was less effective than pasireotide. Tamoxifen inhibited hyperplasia when used alone with GH + E2, but did not add to the inhibitory effect of pasireotide when the two treatments were combined. Both pasireotide and tamoxifen acted via the IGF-I receptor signaling pathway and both were found to inhibit mammary cell proliferation and stimulate apoptosis. The number of epithelial cells expressing phosphorylated insulin receptor substrate (IRS)-1 in response to GH and E2 was reduced by pasireotide, as was staining intensity. These results support the concept that IGF-I inhibition, in this case by pasireotide, inhibits E2 and GH-induced mammary hyperplasia. As tamoxifen did not further increase the inhibitory effect of pasireotide, the peptide appears to be at least as effective as tamoxifen in preventing GH + E2-induced mammary hyperplasia
Alternative approach to insulin-like growth factor-1 inhibition for treatment of breast cancer.
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Severe bone disease with bilateral femur fracture in a young woman after gastrectomy for gastric polyposis with SMAD4 mutation.
No full textThe Need for Cardiovascular Risk Factor Prevention in Cardio-Oncology
No full textNo abstract availabl
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