Pirfenidone induces intercellular adhesion molecule-1 (ICAM-1) down-regulation on cultured human synovial fibroblasts

Kaneko, Masanori; Inoue, Hiroko; Nakazawa, Ryoichi; Azuma, Nakanobu; Suzuki, Masatsugu; Yamauchi, Shitotomo; Margolin, Solomon B.; Tsubota, Kazuo; Saito, Ichiro

doi:10.1046/j.1365-2249.1998.00618.x

Cited by 66 publications

(54 citation statements)

References 23 publications

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“…7,10,30,[42][43][44] The present results suggest that PFD attenuates CHF-related arrhythmogenic atrial remodeling via a complex set of actions, affecting multiple levels and components of the fibrosis formation and degradation signaling cascade.…”

Section: Effects Of Pirfenidonementioning

confidence: 70%

Pirfenidone Prevents the Development of a Vulnerable Substrate for Atrial Fibrillation in a Canine Model of Heart Failure

et al. 2006

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Background-Atrial fibrosis is an important substrate in atrial fibrillation (AF), particularly in the setting of structural heart disease. In a canine model, congestive heart failure (CHF) produces significant atrial fibrosis and the substrate for sustained AF. This atrial remodeling is a potential therapeutic target. The objective of the present study is to evaluate the effects of the antifibrotic drug pirfenidone (PFD) on arrhythmogenic atrial remodeling in a canine CHF model. Methods and Results-We studied 15 canines, divided equally into 3 groups: control, CHF canines not treated with PFD, and CHF canines treated with PFD. CHF was induced by ventricular tachypacing (220 bpm for 3 weeks), and oral PFD was administered for the 3-week pacing period. We performed electrophysiology and AF vulnerability studies, atrial fibrosis measurements, and atrial cytokine expression studies.

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Section: Effects Of Pirfenidonementioning

confidence: 70%

Pirfenidone Prevents the Development of a Vulnerable Substrate for Atrial Fibrillation in a Canine Model of Heart Failure

et al. 2006

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“…Hale and coworkers reported that pirfenidone reduced staphylococcal enterotoxin B-induced cytokine levels and T-cell proliferation in a murine shock model and in vitro human peripheral blood lymphocyte assays (18). Moreover, pirfenidone induced intracellular adhesion molecule-1 downregulation on cultured human synovial fibroblasts (47). These results suggest that pirfenidone may be promising as a new therapeutic strategy for patients with asthma who have airway structural changes and remodeling in response to persistent inflammation.…”

Section: Discussionmentioning

confidence: 98%

Pirfenidone Modulates Airway Responsiveness, Inflammation, and Remodeling after Repeated Challenge

Hirano

Kanehiro

Ono

et al. 2006

Am J Respir Cell Mol Biol

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We investigated the therapeutic potential of a newly developed antifibrotic agent, pirfenidone, to regulate airway remodeling and the development of allergic airway inflammation and airway hyperresponsiveness after chronic allergen challenge. Administration of pirfenidone after sensitization but during the period of ovalbumin challenge significantly prevented the development of airway hyperresponsiveness and prevented eosinophil and lymphocyte accumulation in the airways. IL-4, IL-5, and IL-13 levels in bronchoalveolar lavage fluid and ovalbumin-specific serum IgE antibody levels were also significantly reduced. Treatment with pirfenidone significantly reduced transforming growth factor-␤1 and platelet-derived growth factor levels in bronchoalveolar lavage fluid. Pirfenidone reduced the expression of transforming growth factor-␤1, the development of goblet cell hyperplasia and subepithelial collagenization, and the increases in contractile elements in the lung. These data indicate that pirfenidone may play an important role in the treatment of asthma and has the potential reduce or prevent airway remodeling.

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“…In addition, it has been shown to lessen pulmonary fibrosis by modulating the fibroproliferative actions of transforming growth factor-β in cultured human fibroblasts [79]. Encouraging results have recently been reported from a double-blind, placebo-controlled study evaluating the treatment effect of pirfenidone in 107 patients with idiopathic pulmonary fibrosis.…”

Section: Treatmentmentioning

confidence: 99%

Pulmonary Fibrosis in Hermansky-Pudlak Syndrome

et al. 2006

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Hermansky-Pudlak syndrome (HPS) is a rare heterogeneously inherited autosomal recessive group of disorders presenting with oculocutaneous albinism, bleeding diathesis and pulmonary disease. HPS is thought to occur as a consequence of disturbed formation or trafficking of intracellular vesicles, most importantly, melanosomes, platelet dense granules and lysosomes. The latter finding, in particular, contributes much to the morbidity associated with the disease, as ceroid lipofuscin deposits in lysosomes affect many organ systems. This is especially problematic in the lungs where it is often associated with pulmonary fibrosis and premature death. Currently, there are 7 known HPS genes in humans. In the mouse, at least 16 known HPS genes produce HPS-mutant phenotypes. The HPS gene mutation is considered to be one of the most prevalent single-gene disorders in northwest Puerto Rico, home to the largest cohort of known patients. In HPS, interventions addressing the bleeding diathesis and pulmonary fibrosis are often disappointingly ineffectual. Pirfenidone, a novel compound with documented anti-inflammatory, antioxidant and antifibrotic effects, appears to hold promise in delaying or preventing fibrosis. To date, there has been one successful lung transplant performed on a patient with HPS. We present a patient with HPS and review the current literature on our understanding of this rare disorder.

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Pirfenidone induces intercellular adhesion molecule-1 (ICAM-1) down-regulation on cultured human synovial fibroblasts

Cited by 66 publications

References 23 publications

Pirfenidone Prevents the Development of a Vulnerable Substrate for Atrial Fibrillation in a Canine Model of Heart Failure

Pirfenidone Prevents the Development of a Vulnerable Substrate for Atrial Fibrillation in a Canine Model of Heart Failure

Pirfenidone Modulates Airway Responsiveness, Inflammation, and Remodeling after Repeated Challenge

Pulmonary Fibrosis in Hermansky-Pudlak Syndrome

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