Severity of peripheral atherosclerosis is associated with fibrinogen and degradation of cross-linked fibrin.

Lassila, Riitta; Peltonen, Seija; Lepäntalo, Mauri; Saarinen, O.; Kauhanen, Petteri; Manninen, Vesa

doi:10.1161/01.atv.13.12.1738

Cited by 126 publications

(82 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…[17][18][19] Increased PAI-1 is associated with all forms of atherothrombosis, 20 -22 and continuous fibrin deposition on the atherosclerotic vessel wall appears to stimulate endogenous fibrinolysis, reflected in elevated t-PA levels. 17 We also found that there was no difference between the patients and healthy age-, sex-, medication-, and cardiovascular risk factor-matched control subjects in resting levels of t-PA to PAI-1 Ag ratio, t-PA-activity, or PAP. In spite of this similarity in fibrinolytic potential measured from plasma, D-dimer was significantly higher in the patients, probably because of the increased amount of preexisting fibrin.…”

Section: Discussionmentioning

confidence: 99%

“…29 At rest, depending on the severity of PAOD in the patients involved, various degrees of activation of the coagulation cascade have been reported previously by our group and others. 17,18 The effect of exercise on hemostasis in patients with peripheral arterial disease has also been studied previously. 19 In contrast to our results, the PAOD patients in the study by Herren et al 19 showed enhanced thrombin formation (TAT) at rest compared with the age-and sex-matched healthy control group.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Physical Exertion Induces Thrombin Formation and Fibrin Degradation in Patients With Peripheral Atherosclerosis

Mustonen

Lepäntalo

Lassila

1998

ATVB

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Physical Exertion Induces Thrombin Formation and Fibrin Degradation in Patients With Peripheral Atherosclerosis

Mustonen

Lepäntalo

Lassila

1998

ATVB

View full text Add to dashboard Cite

show abstract

“…Due to the diverse functions of these proteases and their degradation products, fibrinolytic activity is tightly regulated by a number of protease inhibitors, in particular PAs by plasminogen activator inhibitors (PAIs) and plasmin by the serpin inhibitors, ␣ 2 -antiplasmin, ␣ 1 -antitrypsin, and ␣ 2 -macroglobulin. 5 Although deposition of a fibrin matrix is fundamental to normal repair, it is also a common consequence of a number of pathological disorders such as atherosclerosis, 9 restenosis, 10 postoperative adhesions, 11 pulmonary fibrosis, 12 and tumorigenesis. 13 In such conditions, the presence of fibrin is often integrally associated with excess collagen accumulation and fibrosis.…”

mentioning

confidence: 99%

Fibrin-Induced Skin Fibrosis in Mice Deficient in Tissue Plasminogen Activator

Giorgio-Miller

Bottoms

Laurent

et al. 2005

The American Journal of Pathology

View full text Add to dashboard Cite

The deposition of fibrin is an integral part of the tissue repair process, but its persistence is also associated with a number of fibrotic conditions. This study addressed the hypothesis that reduced fibrinolysis and fibrin persistence are associated with an enhanced accumulation of collagen and the development of skin fibrosis. Decreased fibrinolysis was confirmed in fibrin gel cultures that contained human dermal fibroblasts plus the specific plasmin inhibitor ␣ 2 -antiplasmin or dermal fibroblasts isolated from plasminogen activator (PA)-deficient mice. Collagen accumulation was significantly increased in the presence of inhibitor and in tPA-deficient, but not uPAdeficient, fibroblasts compared with controls. These findings were also confirmed using a skin fibrosis model in which multiple injections of fibrin were given subcutaneously to PA-deficient mice. Injection sites from tPA-deficient mice displayed significantly increased collagen levels compared with uPA-deficient mice and wild-type controls. Up-regulation of fibroblast procollagen gene expression and reduced activation of pro-MMP-1 appeared to mediate the increase in collagen by human dermal fibroblasts in the presence of ␣2-antiplasmin. These findings suggest that persistent fibrin is associated with enhanced collagen accumulation that may result in the development of fibrotic skin disorders in which reduced fibrinolysis is a feature.

show abstract

“…6 Further, both Fg and fibrin have been implicated in the progression of certain types of tumors, 7 and in the severity of atherosclerosis. 8 Congenital afibrinogenemia (MIM no. 202400), an autosomal recessive disorder, was first described in 1920, 9 and since that time more than 150 cases have been reported.…”

mentioning

confidence: 99%

Fibrinogen Stabilizes Placental-Maternal Attachment During Embryonic Development in the Mouse

Iwaki

Sandoval-Cooper

Paiva

et al. 2002

The American Journal of Pathology

View full text Add to dashboard Cite

Fibrinogen (Fg) is a 340-kd symmetrical heterodimeric protein consisting of three pairs of nonidentical polypeptide chains, and has an overall structure of (A␣/B␤/␥) 2 . This protein is the precursor of fibrin, formed during the hemostatic response. Three separate genes, FGA, FGB, and FGG, located on a 50-kb region of chromosome 4q28-q31, are translated in a coordinated fashion to code for the A␣-, B␤-, and ␥-chains, respectively, of Fg. 1 For its conversion into fibrin, thrombin first catalyzes release of fibrinopeptides A and B from the A␣ and B␤ chains, thus leading to exposure of polymerization sites that organize the initially formed fibrin monomers into a polymeric network of fibers that form the major protein component of the blood clot. This clot is ultimately covalently stabilized by crosslinking of specific ⑀-NH 2 groups of Lys and ␥-COOH groups of Glu residues of fibrin monomer, a process catalyzed by a transglutaminase, namely, activated Factor XIII (FXIIIa). 2

show abstract

Severity of peripheral atherosclerosis is associated with fibrinogen and degradation of cross-linked fibrin.

Cited by 126 publications

References 38 publications

Physical Exertion Induces Thrombin Formation and Fibrin Degradation in Patients With Peripheral Atherosclerosis

Physical Exertion Induces Thrombin Formation and Fibrin Degradation in Patients With Peripheral Atherosclerosis

Fibrin-Induced Skin Fibrosis in Mice Deficient in Tissue Plasminogen Activator

Fibrinogen Stabilizes Placental-Maternal Attachment During Embryonic Development in the Mouse

Contact Info

Product

Resources

About