Autoantibody against matrix metalloproteinase-3 in patients with systemic sclerosis

Nishijima, Chihiro; Hayakawa, Ikuko; Matsushita, T.; Komura, Kazuhiro; Hasegawa, Minoru; Takehara, Kazuhiko; Sato, Shinichi

doi:10.1111/j.1365-2249.2004.02615.x

Cited by 81 publications

(50 citation statements)

References 40 publications

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“…One possibility is that the MMPs that normally regulate these chemokines through cleavage are not functioning properly. In support of this, fibrosis resulting from systemic sclerosis may be due to development of function-blocking antibodies to MMP1 and MMP3, allowing deposition of ECM (190).…”

Section: B Interstitial Lung Disease and Idiopathic Pulmonary Fibrosismentioning

confidence: 99%

Matrix Metalloproteinases in Lung: Multiple, Multifarious, and Multifaceted

Greenlee¹,

Werb²,

Kheradmand³

2007

Physiological Reviews

407

330

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The matrix metalloproteinases (MMPs), a family of 25 secreted and cell surface-bound neutral proteinases, process a large array of extracellular and cell surface proteins under normal and pathological conditions. MMPs play critical roles in lung organogenesis, but their expression, for the most part, is downregulated after generation of the alveoli. Our knowledge about the resurgence of the MMPs that occurs in most inflammatory diseases of the lung is rapidly expanding. Although not all members of the MMP family are found within the lung tissue, many are upregulated during the acute and chronic phases of these diseases. Furthermore, potential MMP targets in the lung include all structural proteins in the extracellular matrix (ECM), cell adhesion molecules, growth factors, cytokines, and chemokines. However, what is less known is the role of MMP proteolysis in modulating the function of these substrates in vivo. Because of their multiplicity and substantial substrate overlap, MMPs are thought to have redundant functions. However, as we explore in this review, such redundancy most likely evolved as a necessary compensatory mechanism given the critical regulatory importance of MMPs. While inhibition of MMPs has been proposed as a therapeutic option in a variety of inflammatory lung conditions, a complete understanding of the biology of these complex enzymes is needed before we can reasonably consider them as therapeutic targets.

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Section: B Interstitial Lung Disease and Idiopathic Pulmonary Fibrosismentioning

confidence: 99%

Matrix Metalloproteinases in Lung: Multiple, Multifarious, and Multifaceted

Greenlee¹,

Werb²,

Kheradmand³

2007

Physiological Reviews

407

330

View full text Add to dashboard Cite

show abstract

“…Воздействие антител к фибриллину 1 на фибробласты in vitro приводит к активации клеток через путь, зависимый от трансформирующего фактора роста β (ТФРβ; Smad3), и приобретению ими профиброзного «склеродермическо-го» фенотипа, увеличивая продукцию компонентов вне-клеточного матрикса. Больные ССД также имеют повы-шенные уровни антител к ММП1 и ММП3 -ферментам, участвующим в деградации межклеточного матрикса [117]. Подавляя активность ММП, они способствуют избыточ-ному фиброзообразованию.…”

Section: таблицаunclassified

Autoantibodies in Systemic Sclerosis: Spectrum, Clinical Associations, and Prognostic Value

Ананьева¹,

Александрова²

2016

rsp

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“…Die fibrotischen Prozesse werden von Endothelinen initiiert und verstärkt [17]. Zudem scheinen Antikörper gegen Fibroblasten [18] und Antikörper gegen die kollagenabbauenden Matrixmetalloproteinasen 1 und 3 [19] eine pathogenetische Rolle zu spielen.…”

Section: Pathogeneseunclassified

Therapeutisches Management akraler Manifestationen der systemischen Sklerose

et al. 2007

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Acral manifestations of systemic sclerosis include Raynaud's phenomenon, calcinosis cutis, and sclerodactyly. In the later stages of the disease, contractures of the skin and joints as well as obliterative vasculopathy leading to digital ulcers and necrotic lesions may occur. Patients with acral manifestations of systemic sclerosis are ideally treated by a team that includes a rheumatologist, dermatologist, hand surgeon, physiotherapist, and, eventually, a psychologist. Calcium channel antagonists, alpha(1)-adrenergic blockade with prazosin, and prostacyclin analogs were proven to be effective in the treatment of scleroderma-related Raynaud's phenomenon. Losartan, an angiotensin II receptor inhibitor, and fluoxetine, a selective serotonin reuptake inhibitor, have been beneficial for systemic sclerosis-associated Raynaud's phenomenon in pilot studies. Parenteral prostacyclin analogs, e. g., iloprost, can be recommended as first-line treatment of ischemic digital ulcers. When prostacyclin analogs fail, the phosphodiesterase type 5 inhibitor sildenafil can be tried to improve ulcer healing. Bosentan, an endothelin receptor antagonist, may prevent new digital ulcers. At present, there are no medical agents agreed to be generally effective in the reduction of calcinotic deposits or cutaneous fibrosis, although some drugs have been identified as potentially beneficial. Surgical treatment of acral manifestations consists of excision or curettage of symptomatic calcific deposits, digital sympathectomy, arterial reconstruction, and amputation in rare cases. Flexion contractures of the proximal interphalangeal joints, with secondary hyperextension of the metacarpophalangeal joints, can be treated by arthrodesis of the proximal interphalangeal joints and resection arthroplasty or prostheses at the metacarpophalangeal joints to improve hand function.

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Autoantibody against matrix metalloproteinase-3 in patients with systemic sclerosis

Cited by 81 publications

References 40 publications

Matrix Metalloproteinases in Lung: Multiple, Multifarious, and Multifaceted

Matrix Metalloproteinases in Lung: Multiple, Multifarious, and Multifaceted

Autoantibodies in Systemic Sclerosis: Spectrum, Clinical Associations, and Prognostic Value

Therapeutisches Management akraler Manifestationen der systemischen Sklerose

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