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351. Cathepsin S contributes to macrophage migration via degradation of elastic fibre integrity to facilitate vein graft neointimal hyperplasia.

352. DHEA inhibits vascular remodeling following arterial injury: a possible role in suppression of inflammation and oxidative stress derived from vascular smooth muscle cells.

353. Transplantation of mesenchymal stem cells carrying the human receptor activity-modifying protein 1 gene improves cardiac function and inhibits neointimal proliferation in the carotid angioplasty and myocardial infarction rabbit model.

354. The transcription factor E26 transformation-specific sequence-1 mediates neointima formation in arteriovenous fistula.

355. Anthocyanidins, novel FAK inhibitors, attenuate PDGF-BB-induced aortic smooth muscle cell migration and neointima formation.

356. DNA aptamer raised against advanced glycation end products inhibits neointimal hyperplasia in balloon-injured rat carotid arteries.

357. Heat shock protein 27 attenuates neointima formation and accelerates reendothelialization after arterial injury and stent implantation: importance of vascular endothelial growth factor up-regulation.

358. Interferon regulatory factor 8 modulates phenotypic switching of smooth muscle cells by regulating the activity of myocardin.

359. Oxidative activation of the Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) regulates vascular smooth muscle migration and apoptosis.

360. Role of metabolic environment on nitric oxide mediated inhibition of neointimal hyperplasia in type 1 and type 2 diabetes.

361. Ras-Mek-Erk signaling regulates Nf1 heterozygous neointima formation.

362. Adipose-derived stem cells stimulate reendothelialization in stented rat abdominal aorta.

364. IL-6 mobilizes bone marrow-derived cells to the vascular wall, resulting in neointima formation via inflammatory effects.

365. Mig-6 gene knockout induces neointimal hyperplasia in the vascular smooth muscle cell.

366. Interleukin-1 receptor antagonist originating from bone marrowderived cells and non-bone marrow-derived cells helps to suppress arterial inflammation and reduce neointimal formation after injury.

367. Bone mesenchymal stem cells contributed to the neointimal formation after arterial injury.

368. The N-glycoform of sRAGE is the key determinant for its therapeutic efficacy to attenuate injury-elicited arterial inflammation and neointimal growth.

369. Saturated fatty acid palmitate aggravates neointima formation by promoting smooth muscle phenotypic modulation.

370. Increasing our IQ of vascular smooth muscle cell migration with IQGAP1. Focus on "IQGAP1 links PDGF receptor-β signal to focal adhesions involved in vascular smooth muscle cell migration: role in neointimal formation after vascular injury".

371. IQGAP1 links PDGF receptor-β signal to focal adhesions involved in vascular smooth muscle cell migration: role in neointimal formation after vascular injury.

372. FK506 activates BMPR2, rescues endothelial dysfunction, and reverses pulmonary hypertension.

373. Inhibition of patched-1 prevents injury-induced neointimal hyperplasia.

374. Inhibition of reactive oxygen species generation attenuates TLR4-mediated proinflammatory and proliferative phenotype of vascular smooth muscle cells.

375. The microRNA miR-132 targets Lrrfip1 to block vascular smooth muscle cell proliferation and neointimal hyperplasia.

376. Leptin promotes neointima formation and smooth muscle cell proliferation via NADPH oxidase activation and signalling in caveolin-rich microdomains.

377. Essential role of Pin1 via STAT3 signalling and mitochondria-dependent pathways in restenosis in type 2 diabetes.

378. Cinaciguat prevents neointima formation after arterial injury by decreasing vascular smooth muscle cell migration and proliferation.

380. Cyclooxygenase-2-derived prostaglandin E₂ promotes injury-induced vascular neointimal hyperplasia through the E-prostanoid 3 receptor.

381. TLR accessory molecule RP105 (CD180) is involved in post-interventional vascular remodeling and soluble RP105 modulates neointima formation.

382. Sulforaphane inhibits PDGF-induced proliferation of rat aortic vascular smooth muscle cell by up-regulation of p53 leading to G1/S cell cycle arrest.

383. Modelling the effect of a functional endothelium on the development of in-stent restenosis.

384. D-series resolvin attenuates vascular smooth muscle cell activation and neointimal hyperplasia following vascular injury.

385. Monocyte chemoattractant protein 1-mediated migration of mesenchymal stem cells is a source of intimal hyperplasia.

387. Cortistatin inhibits migration and proliferation of human vascular smooth muscle cells and decreases neointimal formation on carotid artery ligation.

388. Over-expression of neuron-derived orphan receptor-1 (NOR-1) exacerbates neointimal hyperplasia after vascular injury.

389. Knockout of CD8 delays reendothelialization and accelerates neointima formation in injured arteries of mouse via TNF-α inhibiting the endothelial cells migration.

390. Compound K, an intestinal metabolite of ginsenosides, inhibits PDGF-BB-induced VSMC proliferation and migration through G1 arrest and attenuates neointimal hyperplasia after arterial injury.

391. A repressor protein, Mnt, is a novel negative regulator of vascular smooth muscle cell hypertrophy by angiotensin II and neointimal hyperplasia by arterial injury.

392. Endogenous cannabinoid receptor CB1 activation promotes vascular smooth-muscle cell proliferation and neointima formation.

393. Antagonistic effect of C19 on migration of vascular smooth muscle cells and intimal hyperplasia induced by chemokine-like factor 1.

394. Perivascular adipose tissue-secreted angiopoietin-like protein 2 (Angptl2) accelerates neointimal hyperplasia after endovascular injury.

395. Targeted STIM deletion impairs calcium homeostasis, NFAT activation, and growth of smooth muscle.

396. Cell division fidelity is altered during the vascular response to injury: its novel role in atherosclerosis progression.

397. Protective effect of nectandrin B, a potent AMPK activator on neointima formation: inhibition of Pin1 expression through AMPK activation.

398. Increased expression of hypoxia-inducible factor-1α in proliferating neointimal lesions in a rat model of pulmonary arterial hypertension.

399. Crucial role of hyaluronan in neointimal formation after vascular injury.

400. Lithium chloride inhibits vascular smooth muscle cell proliferation and migration and alleviates injury-induced neointimal hyperplasia via induction of PGC-1α.

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