Last update 01 Nov 2024

ANGPTL7

Last update 01 Nov 2024

Basic Info

Synonyms

angiopoietin like 7, Angiopoietin-like factor, Angiopoietin-like protein 7

+ [5]

Introduction

Has a role in the formation and organization of the extracellular matrix. In the eye, it functions as a mediator of dexamethasone-induced matrix deposition in the trabecular meshwork, the tissue responsible for the outflow of the ocular aqueous humor and for the maintenance of intraocular pressure (PubMed:21199193). Is a negative regulator of angiogenesis in the cornea, and plays a major role in maintaining corneal avascularity and transparency (PubMed:25622036).

Drugs associated with ANGPTL7

ANGPTL7 siRNA(ALNYLAM)

Target

ANGPTL7

Mechanism

ANGPTL7 modulators

Active Org.

Regeneron Pharmaceuticals, Inc. [+1]

Originator Org.

Regeneron Pharmaceuticals, Inc. [+1]

Active Indication

Glaucoma

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Glaucoma therapy (Maze Therapeutics)

Target

ANGPTL7

Mechanism

ANGPTL7 modulators

Active Org.

Maze Therapeutics, Inc.Startup

Originator Org.

Maze Therapeutics, Inc.Startup

Active Indication

Glaucoma

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with ANGPTL7

100 Translational Medicine associated with ANGPTL7

0 Patents (Medical) associated with ANGPTL7

160

Literatures (Medical) associated with ANGPTL7

01 Oct 2024·Ecotoxicology and Environmental Safety

The pro-atherogenic effects and the underlying mechanisms of chronic bisphenol S (BPS) exposure in apolipoprotein E-deficient mice

Article

Author: Zuo, Ying-Bing ; Xu, Hai-Ming ; Zhang, Yin-Feng ; Wen, Zeng-Jin ; Yang, Hong-Yu ; Zhang, Yi-Fei ; Xin, Hui ; Jia, Dong-Dong ; Cheng, Meng-Die

Atherosclerosis (AS) and its related cardiovascular diseases (CVDs) remain the most frequent cause of morbidity and mortality worldwide. Researches showed that bisphenol A (BPA) exposure might exacerbate AS progression. However, as an analogue of BPA, little is known about the cardiovascular toxicity of bisphenol S (BPS), especially whether BPS exposure has the pro-atherogenic effects in mammals is still unknown. Here, we firstly constructed an apolipoprotein E knockout (ApoE^-/-) mouse model and cultured cells to investigate the risk of BPS on AS and explore the underlying mechanisms. Results showed that prolonged exposure to 50 μg/kg body weight (bw)/day BPS indeed aggravated AS lesions both in the en face aortas and aortic sinuses of ApoE^-/- mice. Moreover, BPS were found to be implicated in the AS pathological process: 1) stimulates adhesion molecule expression to promote monocyte-endothelial cells (ECs) adhesion with 3.6 times more than the control group in vivo; 2) increases the distribution of vascular smooth muscle cells (VSMCs) with 9.3 times more than the control group in vivo, possibly through the migration of VSMCs; and 3) induces an inflammatory response by increasing the number of macrophages (MACs), with 3.7 times more than the control group in vivo, and the release of inflammatory mediators. Furthermore, we have identified eight significant AS-related genes induced by BPS, including angiopoietin-like protein 7 (Angptl17) and lipocalin-2 (Lcn2) in ECs; matrix metalloproteinase 9 (Mmp13), secreted phosphoprotein 1 (Spp1), and collagen type II alpha 1 (Col2a1) in VSMCs; and kininogen 1 (Kng1), integrin alpha X (Itgax), and MAC-expressed gene 1 (Mpeg1) in MACs. Overall, this study firstly found BPS exposure could exacerbate mammalian AS and might also provide a theoretical basis for elucidating BPS and its analogues induced AS and related CVDs.

09 Sep 2024·Current medicinal chemistry

ANGPTL4-the Link Binding Lipid Metabolism and Inflammation.

Article

Author: Zuo, Yuyue ; Liang, Jingwen ; Dai, Lei ; Li, Zhi ; Zhang, Yueqi

BACKGROUNDAngiopoietin-like 4 (ANGPTL4) belongs to the family of angiopoietin- like proteins. The involvement of ANGPTL4 in various aspects of lipid metabolism and inflammation has become an important area of research.METHODSA thorough search on PubMed related to ANGPTL4, lipid metabolism, and inflammation was performed.RESULTSOver the past two decades, the recognition of ANGPTL4 as a potent regulator of lipid metabolism has substantially increased. As part of the senescence-associated secretory phenotype, ANGPTL4 also serves as an inflammatory mediator. Considering the advancements in ANGPTL4 research, we have highlighted that ANGPTL4 acts as a key node linking lipid metabolism and inflammation. ANGPTL4 impacts inflammation by regulating lipid metabolism. It affects critical enzymes (lipoprotein lipase, hepatic lipase, endothelial lipase, and acetyl-CoA carboxylase), regulatory factors (AMPK, cAMP, SLC7A11, GPX4, and mTOR), and receptors (LepR, CD36, and PPARγ) of lipid oxidation, synthesis, and peroxidation, thereby affecting immune cells and inflammatory pathways.CONCLUSIONUnderstanding the potential association and the therapeutic value of ANGPTL4 for regulating lipid metabolism and inflammation could contribute to drug discovery and therapeutic development.

22 Aug 2024·JCI insight

Postprandial exercise regulates tissue-specific triglyceride uptake through angiopoietin-like proteins.

Article

Author: Huang, Kun ; Li, Lin ; Li, Quan ; Liu, Yong ; Han, Bingqian ; Wang, Yan ; Kang, Shijia ; Li, Ying ; Song, Bao-Liang ; Liu, Xiaomin ; Ma, Yifan ; Zhang, Yiliang ; Kong, Lingkai

Fuel substrate switching between carbohydrates and fat is essential for maintaining metabolic homeostasis. During aerobic exercise, the predominant energy source gradually shifts from carbohydrates to fat. While it is well known that exercise mobilizes fat storage from adipose tissues, it remains largely obscure how circulating lipids are distributed tissue-specifically according to distinct energy requirements. Here, we demonstrate that aerobic exercise is linked to nutrient availability to regulate tissue-specific activities of lipoprotein lipase (LPL), the key enzyme catabolizing circulating triglyceride (TG) for tissue uptake, through the differential actions of angiopoietin-like (ANGPTL) proteins. Exercise reduced the tissue binding of ANGPTL3 protein, increasing LPL activity and TG uptake in the heart and skeletal muscle in the postprandial state specifically. Mechanistically, exercise suppressed insulin secretion, attenuating hepatic Angptl8 transcription through the PI3K/mTOR/CEBPα pathway, which is imperative for the tissue binding of its partner ANGPTL3. Constitutive expression of ANGPTL8 hampered lipid utilization and resulted in cardiac dysfunction in response to exercise. Conversely, exercise promoted the expression of ANGPTL4 in white adipose tissues, overriding the regulatory actions of ANGPTL8/ANGPTL3 in suppressing adipose LPL activity, thereby diverting circulating TG away from storage. Collectively, our findings show an overlooked bifurcated ANGPTL-LPL network that orchestrates fuel switching in response to aerobic exercise.

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ANGPTL7

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