Cathepsin L is significantly associated with apoptosis and plaque destabilization in human atherosclerosis

Li, Wei; Kornmark, Louise; Jonasson, Lena; Forssell, Claes; Yuan, Xi

doi:10.1016/j.atherosclerosis.2008.03.027

Cited by 87 publications

(66 citation statements)

References 34 publications

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“…Based on our in vitro results showing that inhibition of cathepsin L blocked monocyte adhesion to endothelial cells, we speculate that monocyte cathepsin L is critical for adhesion and infiltration of those cells into the arterial wall. This role of cathepsin L might also be important for the observation that cathepsin L contributes to destabilization of human atherosclerotic plaques (26,27). Whether the higher expression of cathepsins in atherosclerotic plaques could contribute to the exaggerated IH response seen in models of atherosclerosis is an interesting possibility.…”

Section: Cathepsin L Activity Assaymentioning

confidence: 99%

Cathepsin L Promotes Vascular Intimal Hyperplasia after Arterial Injury

Cai

Zhong

et al. 2017

Mol Med

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The inflammatory pathways that drive the development of intimal hyperplasia (IH) following arterial injury are not fully understood. We hypothesized that the lysosomal cysteine protease cathepsin L activates processes leading to IH after arterial injury. Using a mouse model of wire-induced carotid artery injury, we showed that cathepsin L activity peaks at d 7 and remains elevated for 28 d. Genetic deletion of cathepsin L prevented IH and monocyte recruitment in the carotid wall. The injury-induced increases in cathepsin L mRNA and activity were mitigated in mice with myeloid-specific deletion of toll-like receptor 4 (TLR4) or myeloid differentiation primary response gene 88 (MyD88). We further discovered that the HIV protease inhibitor saquinavir (SQV), which is known to block recombinant mouse cathepsin L activity in vitro, prevented IH after arterial injury. SQV also suppressed LPS (TLR4 agonist)-induced monocyte adhesion to endothelial monolayers. These findings establish cathepsin L as a critical regulator of the inflammation that leads to IH and that the TLR4-MyD88 pathway in myeloid lineages regulates cathepsin L expression in the vessel wall following wire injury. The Food and Drug Administration-approved drug SQV blocks IH though mechanisms that may include the suppression of cathepsin L.

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Section: Cathepsin L Activity Assaymentioning

confidence: 99%

Cathepsin L Promotes Vascular Intimal Hyperplasia after Arterial Injury

Cai

Zhong

et al. 2017

Mol Med

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“…Serum cathepsin L level correlated with the development of atherosclerotic lesions . Furthermore, expression of cathepsin L correlated with apoptosis, formation of the necrotic core, decrease in collagen content and rupture of the fibrous cap (Li et al, 2009;Liu et al, 2006).…”

Section: Atherosclerosismentioning

confidence: 95%

“…The activities of cathepsin S and L were increased in abdominal aortic aneurysms and ruptured abdominal aortic aneurysms, whereas cathepsin K activity was not elevated despite a significant increase in the level of activated cathepsin K protein in aortic extracts (Abdul-Hussien et al, 2007;Abisi et al, 2007). Increased expression of cathepsin L in abdominal aortic aneurysm was localized in SMCs, Ecs and macrophages (Li et al, 2009). …”

Section: Aortic Aneurysmmentioning

confidence: 99%

Role of Cathepsin K, L and S in Blood Vessel Remodeling

Samokhin¹,

Brὂmme²

2011

Aneurysmal Disease of the Thoracic and Abdominal Aorta

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“…Cytosolic cytochrome c then promotes caspase activation through apoptosome formation. Activation of these classical pathways has been shown to occur in macrophages with experimental evidence implicating the following: Bim [92], Bax [93], FasL [94], caspases [95], p53 [96], Poly (ADP-ribose) polymerase (PARP)-1 [97], peroxisome proliferator-activated receptor (PPAR)-a/c [98], migration inhibitory factor (MIF) [99], matrix metallo-proteinases (MMPs) [100], Cathepsin L/K [101,102], lipoprotein-associated phospholipase A2 (Lp-PLA2) [103], ox-LDL [104] and oxysterols [105].…”

Section: Macrovascular Complications-cardiovascular Disease and Macromentioning

confidence: 99%

Diabetes mellitus and apoptosis: inflammatory cells

et al. 2009

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Since the early observation that similarities between thyroiditis and insulitis existed, the important role played by inflammation in the development of diabetes has been appreciated. More recently, experiments have shown that inflammation also plays a prominent role in the development of target organ damage arising as complications, with both elements of the innate and the adaptive immune system being involved, and that cytokines contributing to local tissue damage may arise from both infiltrating and resident cells. This review will discuss the experimental evidence that shows that inflammatory cellmediated apoptosis contributes to target organ damage, from beta cell destruction to both micro-and macro-vascular disease complications, and also how alterations in leukocyte turnover affects immune function.

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Cathepsin L is significantly associated with apoptosis and plaque destabilization in human atherosclerosis

Cited by 87 publications

References 34 publications

Cathepsin L Promotes Vascular Intimal Hyperplasia after Arterial Injury

Cathepsin L Promotes Vascular Intimal Hyperplasia after Arterial Injury

Role of Cathepsin K, L and S in Blood Vessel Remodeling

Diabetes mellitus and apoptosis: inflammatory cells

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