Activation of PPARδ prevents endothelial dysfunction induced by overexpression of amyloid-β precursor protein

نویسندگان
چکیده

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Activation of PPARd prevents endothelial dysfunction induced by overexpression of amyloid-b precursor protein

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Activation of PPARd prevents endoth...

متن کامل

Mitochondrial aldehyde dehydrogenase-2 activation prevents β-amyloid-induced endothelial cell dysfunction and restores angiogenesis.

Amyloid β peptides (Aβ1-40 and Aβ1-42) cause cerebral degeneration by impairing the activity of angiogenic factors and inducing apoptosis and senescence in the endothelium. Amyloid peptides are known to induce oxidative stress. Impairment of mitochondrial aldehyde dehydrogenase 2 (ALDH2) following oxidative stress, results in accumulation of toxic aldehydes, particularly 4-hydroxynoneal (4-HNE)...

متن کامل

Overexpression of CuZn-SOD prevents lipopolysaccharide-induced endothelial dysfunction.

BACKGROUND AND PURPOSE Inflammation is thought to be a major contributor to carotid artery disease. Lipopolysaccharide (LPS) activates inflammatory mechanisms thought to contribute to endothelial dysfunction by mechanisms that are not well defined. The goal of this study was to determine whether overexpression of CuZn-SOD protects against LPS-induced increases in superoxide and endothelial dysf...

متن کامل

Minocycline blocks c-terminal fragments of amyloid precursor protein-induced neurotoxicity by inhibition of cytochrome c release and caspase-12 activation

Minocycline is a second-generation tetracycline that effectively crosses the blood-brain barrier. It has remarkable neuroprotective qualities in models of cerebral ischaemia, traumatic brain injury, Huntington’s and Parkinson’s diseases. However, there is no evidence about neuroprotective effects of minocycline on AD. Alzheimer’s disease (AD) is a neurodegenerative disorder characterized neurop...

متن کامل

Minocycline blocks c-terminal fragments of amyloid precursor protein-induced neurotoxicity by inhibition of cytochrome c release and caspase-12 activation

Minocycline is a second-generation tetracycline that effectively crosses the blood-brain barrier. It has remarkable neuroprotective qualities in models of cerebral ischaemia, traumatic brain injury, Huntington’s and Parkinson’s diseases. However, there is no evidence about neuroprotective effects of minocycline on AD. Alzheimer’s disease (AD) is a neurodegenerative disorder characterized neurop...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

ژورنال

عنوان ژورنال: Cardiovascular Research

سال: 2012

ISSN: 1755-3245,0008-6363

DOI: 10.1093/cvr/cvs266