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10.1007/s00441-011-1189-3 http://scihub22266oqcxt.onion/10.1007/s00441-011-1189-3 C4915479!4915479!21626289     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Tissue+Res 2012 ; 347 (1): 155-75 Nephropedia Template TP {{tp|p=21626289|t=2012. Transforming growth factor-? and atherosclerosis: interwoven atherogenic and atheroprotective aspects |pdf=|usr=}}{{21626289}} gab.com Text Transforming growth factor- and atherosclerosis: interwoven atherogenic and atheroprotective aspects JO: Cell Tissue Res http://www.kidney.de/pget.php?&tw=1&pmid=21626289 #FOAvip Age-related progression of cardiovascular disease is by far the largest health problem in the US and involves vascular damage, progressive vascular fibrosis and the accumulation of lipid-rich atherosclerotic lesions. Advanced lesions can restrict flow to key organs and can trigger occlusive thrombosis resulting in a stroke or myocardial infarction. Transforming growth factor-beta (TGF-?) is a major orchestrator of the fibroproliferative response to tissue damage. In the early stages of repair, TGF-? is released from platelets and activated from matrix reservoirs; it then stimulates the chemotaxis of repair cells, modulates immunity and inflammation and induces matrix production. At later stages, it negatively regulates fibrosis through its strong antiproliferative and apoptotic effects on fibrotic cells. In advanced lesions, TGF-? might be important in arterial calcification, commonly referred to as ?hardening of the arteries?. Because TGF-? can signal through multiple pathways, namely the SMADs, a MAPK pathway and the Rho/ROCK pathways, selective defects in TGF-? signaling can disrupt otherwise coordinated pathways of tissue regeneration. TGF-? is known to control cell proliferation, cell migration, matrix synthesis, wound contraction, calcification and the immune response, all being major components of the atherosclerotic process. However, many of the effects of TGF-? are essential to normal tissue repair and thus, TGF-? is often thought to be ?atheroprotective?. The present review attempts to parse systematically the known effects of TGF-? on both the major risk factors for atherosclerosis and to isolate the role of TGF-? in the many component pathways involved in atherogenesis. Twit Text FOAVip Transforming growth factor- and atherosclerosis: interwoven atherogenic and atheroprotective aspects ????Cell Tissue Res http://www.kidney.de/pget.php?&tw=1&pmid=21626289 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=21626289 #FOAvip English Wikipedia <ref>{{Cite pmid|21626289}}</ref> Transforming growth factor-? and atherosclerosis: interwoven atherogenic and atheroprotective aspects #MMPMID21626289 Toma I; McCaffrey TA Cell Tissue Res 2012[Jan]; 347 (1): 155-75 PMID21626289show ga Age-related progression of cardiovascular disease is by far the largest health problem in the US and involves vascular damage, progressive vascular fibrosis and the accumulation of lipid-rich atherosclerotic lesions. Advanced lesions can restrict flow to key organs and can trigger occlusive thrombosis resulting in a stroke or myocardial infarction. Transforming growth factor-beta (TGF-?) is a major orchestrator of the fibroproliferative response to tissue damage. In the early stages of repair, TGF-? is released from platelets and activated from matrix reservoirs; it then stimulates the chemotaxis of repair cells, modulates immunity and inflammation and induces matrix production. At later stages, it negatively regulates fibrosis through its strong antiproliferative and apoptotic effects on fibrotic cells. In advanced lesions, TGF-? might be important in arterial calcification, commonly referred to as ?hardening of the arteries?. Because TGF-? can signal through multiple pathways, namely the SMADs, a MAPK pathway and the Rho/ROCK pathways, selective defects in TGF-? signaling can disrupt otherwise coordinated pathways of tissue regeneration. TGF-? is known to control cell proliferation, cell migration, matrix synthesis, wound contraction, calcification and the immune response, all being major components of the atherosclerotic process. However, many of the effects of TGF-? are essential to normal tissue repair and thus, TGF-? is often thought to be ?atheroprotective?. The present review attempts to parse systematically the known effects of TGF-? on both the major risk factors for atherosclerosis and to isolate the role of TGF-? in the many component pathways involved in atherogenesis. äTransforming growth factor-? and atherosclerosis: interwoven atherogen(epmc).pdf DeepDyve Pubget Overpricing