Extracellular Matrix Remodeling in Takayasu's Arteritis: Role of Matrix Metalloproteinases and Adventitial Inflammation

Mahajan, Nitin; Dhawan, Veena; Mahmood, Safrun; Malik, Sonal; Jain, Sanjay

doi:10.1016/j.arcmed.2012.07.007

Cited by 22 publications

(20 citation statements)

References 26 publications

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“…In corroboration, increased serum levels of MMPs and gelatinolytic activities of MMPs have been demonstrated in TA subjects [14, 17, 44–47]. Various cytokines and chemokines, like interleukin-6 (IL-6), regulated on activation normal T cell expressed and secreted (RANTES), and monocytic chemotactic protein-1 (MCP-1), are reported to increase in patients with TA and therefore could possibly accelerate the production of MMPs by inflammatory [16, 47, 48].…”

Section: Mmp-timp Axis In Pathophysiology Of Takayasu's Arteritismentioning

confidence: 63%

“…In an important in vitro study, Mahajan et al demonstrated that a direct contact between activated T-lymphocytes (isolated from TA subjects) and HT1080 fibroblast leads to enhanced expression of MMPs. Subcellular fractionation studies with T cells isolated from TA subjects pointed out the presence of some unidentified antigenic moiety in membrane fraction which is responsible for the enhanced expression of MMPs by HT1080 cells [44]. Therefore, interaction of different cells in the adventitial setting generates a microenvironment which channelizes cells to invade the media and intima through adventitia due to augmented MMP expression.…”

Section: Mmp-timp Axis In Pathophysiology Of Takayasu's Arteritismentioning

confidence: 99%

“…Finding enhanced transcriptional expression of MMPs in TA subjects as compared to normal healthy controls, Mahajan et al emphasized the fact that extracellular matrix remodeling is activated in TA disease, thus making these subjects highly vulnerable to atherosclerosis and development of its related manifestations and aneurysms [44]. In corroboration, increased serum levels of MMPs and gelatinolytic activities of MMPs have been demonstrated in TA subjects [14, 17, 44–47].…”

Section: Mmp-timp Axis In Pathophysiology Of Takayasu's Arteritismentioning

confidence: 99%

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Acknowledged Signatures of Matrix Metalloproteinases in Takayasu’s Arteritis

Mahajan

Dhawan

2014

BioMed Research International

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Takayasu's arteritis (TA) was reported as an eye disease in the year 1905 and later was confirmed as a vasculitis. Since then, the etiology of the disease remains unknown; however, characteristic clinical features suggest multiple causative factors. Recent progress in vascular biology and other disciplines enlightens the pathophysiology of TA and demonstrated induction of various nonspecific inflammatory symptoms and destruction of the arterial wall, which leads to aneurysms and rupture of the affected arteries. Matrix metalloproteinases (MMPs) as an enzyme family have well-established roles in several vascular pathologies including intima formation, atherosclerosiss and aneurysms. MMPs have been proposed to be one of the molecules with a potential of having dual role in the course of TA, first as an active participant in pathophysiology and secondly as a diagnostic biomarker for TA disease. The desire to improve our understanding of the importance of MMPs and their endogenous inhibitors (TIMPs) in TA disease and for the development of therapeutic agents has inspired basic and clinical scientists for over a decade. In the present paper, we summarized the scientific rationale which highlights the signatures of matrix metalloproteinases and their endogenous inhibitors in pathophysiology as well as their being a potential candidate as biomarker for Takayasu's arteritis.

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Section: Mmp-timp Axis In Pathophysiology Of Takayasu's Arteritismentioning

confidence: 63%

Section: Mmp-timp Axis In Pathophysiology Of Takayasu's Arteritismentioning

confidence: 99%

Section: Mmp-timp Axis In Pathophysiology Of Takayasu's Arteritismentioning

confidence: 99%

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Acknowledged Signatures of Matrix Metalloproteinases in Takayasu’s Arteritis

Mahajan

Dhawan

2014

BioMed Research International

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“…There is much evidence that matrix metalloproteinases (MMPs) are involved in the balance between the breakdown and synthesis of extracellular matrix, which determines the risk of rupture of plaques and subsequent disease events [7,43]. MMPs and their inhibitors (TIMPs) have already been demonstrated as potential factors in the pathophysiology of various disease settings [43][44][45][46].…”

Section: Interleukin 18 As Biomarker In Atherosclerosismentioning

confidence: 99%

“…It is generally accepted that a complex endothelial dysfunction induced by free radicals, low-density lipoproteins (LDL), infectious microorganism, shear stress, toxins, hypertension or a combination of these and other factors lead to the development of atherosclerosis. Besides implication of inflammation and immune reactions in this process, a wide range of circulating markers of inflammation has also been demonstrated to predict cardiovascular event in a variety of clinical settings [1,3,4,[6][7][8].…”

Section: Introductionmentioning

confidence: 99%

Interleukin-18 and Atherosclerosis: Mediator or Biomarker

Mahajan¹

2014

J Clin Exp Cardiolog

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Atherosclerosis, a progressive disorder of the vessel walls with the formation of plaques throughout the arterial system, is an essential pathological process in the development of various Cardiovascular Diseases (CVDs). Inflammation has been demonstrated to play an inevitable role in all the stages of atherosclerosis though its pathogenesis is complicated and still remains enigmatic. Interleukin-18 (IL-18) is a pleiotropic pro-inflammatory cytokine, which belongs to the Interleukin-1 (IL-1) family. This pro-inflammatory cytokine is among the more recently recognized cytokines to be involved in the development of various cardiovascular diseases and their related manifestations. At one end, studies indicate that IL-18 is a key player that orchestrates the inflammatory cascade associated with the pathogenesis of atherosclerosis, whereas others showed circulating levels of IL-18 to be a prognostic marker. Present article summarizes the scientific rationale which highlights the signatures of interleukin-18 as a mediator in the pathogenesis as well as a diagnostic marker.

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