1 -) mice, indicating that metformin exerts an
antiatherosclerotic action in vivo via the AMPK-mediated
2 dinediones have been shown to exert multiple
antiatherosclerotic actions in diabetic patients.
3 Nitric oxide has both antithrombotic and
antiatherosclerotic actions in the vasculature, yet its
4 ects of L-arginine by L-NA suggests that the
antiatherosclerotic actions of L-arginine are mediated b
5 The potential
antiatherosclerotic actions of NO were investigated in f
6 ortant target for the antiproliferative, and
antiatherosclerotic actions of PPARgamma ligands.
7 key mediators in flow anti-inflammatory and
antiatherosclerotic actions.
8 Design of shorter, smaller trials of
antiatherosclerotic agents is justified.
9 patients with type 2 diabetes and also have
antiatherosclerotic and antihypertensive effects.
10 Taken together with previously established
antiatherosclerotic and antithrombotic effects, these fi
11 We have previously shown
antiatherosclerotic and vasculoprotective effects of rec
12 raise HDL-C in animals and humans and may be
antiatherosclerotic by enhancing reverse cholesterol tra
13 is a viable strategy for the development of
antiatherosclerotic compounds.
14 Thus, HDCA is a candidate for
antiatherosclerotic drug therapy.
15 In addition, treatment with statin, an
antiatherosclerotic drug, inhibited YAP/TAZ activities t
16 value as a surrogate tool for development of
antiatherosclerotic drugs and noninvasive assessment of
17 Antiatherosclerotic drugs may be exerting some of their
18 in clinical research for the development of
antiatherosclerotic drugs.
19 herosclerosis would assist in the testing of
antiatherosclerotic drugs.
20 vivo is important for the development of new
antiatherosclerotic drugs.
21 letion of Nox1, but not Nox4, had a profound
antiatherosclerotic effect correlating with reduced reac
22 parently disparate observations are that the
antiatherosclerotic effect of CETP inhibition varies wit
23 ese results improve our understanding of the
antiatherosclerotic effect of drugs.
24 on in vascular walls and contribute to their
antiatherosclerotic effect.
25 DPP-4i exerts
antiatherosclerotic effects and reduces inflammation via
26 The antidiabetic and
antiatherosclerotic effects of adiponectin make it a des
27 larly cell-associated proteins, and that the
antiatherosclerotic effects of antioxidants seen in some
28 Mechanistically, the renoprotective and
antiatherosclerotic effects of DMAG are mediated by the
29 servation of SOD may be common mechanisms of
antiatherosclerotic effects of lovastatin, vitamin E and
30 responsible for their anti-inflammatory and
antiatherosclerotic effects remain largely unknown.
31 olesterol absorption with ezetimibe promotes
antiatherosclerotic effects through increased LDL choles
32 rdial protection, insulin-sensitization, and
antiatherosclerotic effects.
33 3) to analyze its potential antidiabetic and
antiatherosclerotic effects.
34 In some animal models, ACAT inhibitors have
antiatherosclerotic effects.
35 erone by blocking its receptor has potential
antiatherosclerotic effects.
36 y, biochemistry and molecular biology of the
antiatherosclerotic enzyme paraoxonase 1.
37 It also directly inactivates 2 critical
antiatherosclerotic enzymes, endothelial nitric oxide sy
38 This HDL-raising effect is
antiatherosclerotic in moderately severe hyperlipidemia
39 de insights into the therapeutic efficacy of
antiatherosclerotic interventions.
40 ndary prevention, including antiplatelet and
antiatherosclerotic medications.
41 Interventions that raise HDL are
antiatherosclerotic,
presumably through acceleration of
42 atherosclerosis and whether IL-10 exerts its
antiatherosclerotic properties by modulating lipid metab
43 Although they possess
antiatherosclerotic properties in vivo and promote endot
44 However, other
antiatherosclerotic properties of HDL are poorly underst
45 thase (eNOS) has been considered to exert an
antiatherosclerotic role through synthesis of NO.
46 racterized by reduced bioavailability of the
antiatherosclerotic signaling molecule nitric oxide (NO)
47 dothelial NO synthase (eNOS) to generate the
antiatherosclerotic signaling radical NO.
48 therapies, supports the need to develop new
antiatherosclerotic strategies in diabetic patients.
49 e potential to predict the efficacy of novel
antiatherosclerotic therapeutics by using a relatively s
50 ular intervention but it has been hoped that
antiatherosclerotic therapies might result in a reductio
51 imaging with IVUS in the evaluation of novel
antiatherosclerotic therapies.
52 as responsiveness of individual patients to
antiatherosclerotic therapies.
53 ntly assist rapid evaluation of experimental
antiatherosclerotic therapies.
54 therogenic agent, and they highlight a novel
antiatherosclerotic therapy using a simple, yet effectiv
55 ity, and reveals the coexistence of pro- and
antiatherosclerotic transcript profiles in susceptible r
56 their use in preventing CIN apart from their
antiatherosclerotic use.