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The Study

ANGPTL7, a therapeutic target for increased intraocular pressure and glaucoma

In simple terms

This study found that people born with certain tiny changes in their ANGPTL7 gene tend to have lower eye pressure and less glaucoma. It’s like noticing that kids who eat more carrots have better vision—but it doesn’t prove carrots cause better vision. The researchers also tested this in mice and saw similar results, which is exciting but doesn’t guarantee it works the same way in people.

63%

Analysis score

63/ 72

Maximum 72 for a cohort study.

Where the score came from

Reporting40
Methodology44
Publication100
Statistical77
Study type (basis of the score)
Cohort Study
Level 2b - Individual cohort study
What’s the bottom line?

Scientists found that people with certain broken versions of a gene called ANGPTL7 have lower eye pressure and less glaucoma. They tested this in mice and found that turning off the gene lowers eye pressure, even in adults.

Where does this study sit?

Reviews of RCTs (Meta-analyses)

Max 100

Randomized Trials

Max 90

Reviews of Cohort Studies

Max 85

Cohort Studies

Max 72

Reviews of Case-Control Studies

Max 63

Case-Control Studies

Max 58

Cross-Sectional & Case Series

Max 50

Expert Opinion

Max 5
StrongerWeaker
Cohort Studies
Level 2b
63

63 / 100

Quality score

Groups of people are followed over time to see who develops an outcome. Strong for identifying risk factors and associations, but cannot prove causation as firmly as RCTs.

Cannot establish causation

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Key takeaways

Summary

Based on the study abstract and findings.

  1. 1A 2–4 mmHg drop in eye pressure is clinically meaningful — it’s similar to the effect of common glaucoma drugs and can significantly reduce blindness risk.
  2. 2People with broken ANGPTL7 genes had 5.2% to 26.5% lower eye pressure; mice without the gene had 11% lower eye pressure; silencing the gene in adult mice lowered pressure by 2–4 mmHg.

Score breakdown, methodology, conflicts of interest, evidence analysis & raw study data

Publication

Journal

Communications Biology

Year

2022

Authors

K. Praveen, Gaurang C. Patel, L. Gurski, Ariane Ayer, Trikaladarshi Persaud, Matthew D. Still, Lawrence Miloscio, Tavé van Zyl, Silvio Alessandro Di Gioia, B. Brumpton, Kristi Krebs, B. Åsvold, Esteban Chen, V. R. Chavali, Wen Fury, H. V. Gudiseva, Sarah Hyde, E. Jorgenson, Stephanie Lefebvre, Dadong Li, Alexander Li, James Mclninch, Brijeshkumar S. Patel, Jeremy S. Rabinowitz, R. Salowe, C. Schurmann, A. Seidelin, Eli Stahl, Dylan Sun, T. Teslovich, A. Tybjærg-Hansen, C. Willer, S. Waldron, Sabrina Walley, Hualing Yang, S. Zaveri, Goncalo R. Michael Andrew Aris Luca A. John D. Jeffrey G. Abecasis Cantor Deubler Economides Lotta Overton R, Goncalo R. Michael Andrew Aris Luca A. John D. Jeffrey G. Abecasis Cantor Deubler Economides Lotta Overton R, Gonçalo R. Abecasis, M. Cantor, Andrew Deubler, A. Economides, L. Lotta, J. Overton, J. Reid, A. Shuldiner, K. Siminovitch, Christina Caitlin Erin D. Zhenhua Michael Alexander Thomas D Beechert Forsythe Fuller Gu Lattari Lopez Schleich, Christina Beechert, Caitlin Forsythe, Erin D. Fuller, Zhenhua Gu, Michael Lattari, Alexander E. Lopez, T. Schleicher, Maria Sotiropoulos Padilla, Louis Widom, Sarah E. Wolf, Manasi Pradhan, Kia Manoochehri, Ricardo Ulloa, Xiaodong Suganthi Suying Boris Siying Gisu Lukas Alicia Sha Bai Balasubramanian Bao Boutkov Chen Eom Habegger , X. Bai, S. Balasubramanian, S. Bao, Boris Boutkov, Siying Chen, Gisu Eom, L. Habegger, A. Hawes, Shareef Khalid, O. Krasheninina, R. Lanche, A. Mansfield, Evan K. Maxwell, Mona Nafde, S. O’Keeffe, Max Orelus, R. Panea, Tommy Polanco, A. Rasool, W. Salerno, Kathie Y. Sun, Amelia Nilanjana Sameer Deepika Jeffery C. Ashish Averitt Banerjee Malhotra Sharma Staples Yadav, A. Averitt, N. Banerjee, S. Malhotra, D. Sharma, Jeff Staples, A. Yadav, Joshua Amy Lee Manuel Allen Revez Arkopravo Christopher H Backman Damask Dobbyn Ferreira Ghosh Gillies Kang , J. Backman, A. Damask, L. Dobbyn, M. Ferreira, A. Ghosh, C. Gillies, H. Kang, Michael D. Kessler, J. Kosmicki, N. Lin, Daren Liu, A. Locke, J. Marchini, A. Marcketta, J. Mbatchou, A. Moscati, C. Paulding, C. Sidore, Kyoko Watanabe, Bin Ye, Blair Zhang, A. Ziyatdinov, Michelle G. Jason Lyndon J. Nirupama Nadia LeBlanc Mighty Mitnaul Nishtala Rana, M. LeBlanc, Jason Mighty, L. Mitnaul, N. Nishtala, N. Rana, Lance J. Jackie Dale Derek Adam David J. Ryan D. F. Dani Adams Blank Bodian Boris Buchanan Carey Colonie Da, Lance J. Adams, J. Blank, D. Bodian, D. Boris, Adam Buchanan, D. Carey, Ryan D. Colonie, F. Davis, Dustin N. Hartzel, Melissa Kelly, H. Kirchner, J. Leader, D. Ledbetter, J. N. Manus, C. Martin, R. Metpally, M. Meyer, T. Mirshahi, M. Oetjens, T. Person, Christopher D. Still, Natasha Strande, Amy Sturm, J. Wagner, Marc Williams, Andres Mari Reedik Tõnu Metspalu Nelis Mägi Esko, A. Metspalu, M. Nelis, R. Mägi, T. Esko, Ying Hu, K. Hveem, O. Melander, L. Milani, S. Stender, Joan M O'Brien, Marcus Jones, Gonçalo R. Abecasis, M. Cantor, J. Weyne, K. Karalis, A. Economides, G. Della Gatta, M. Ferreira, G. Yancopoulos, A. Baras, C. Romano, G. Coppola

Open Access
21 citations
Analysis v6

Related Content

Claims (6)

Assertion

Higher pressure inside the eye directly increases the chance of damage to the optic nerve, and lowering that pressure reduces the risk of such damage.

Causal
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Assertion

In adult mice, injecting a specific RNA molecule into the eye reduces eye pressure by 2–4 mmHg within two weeks by blocking the ANGPTL7 gene product, showing this effect occurs after development and can be reversed by stopping the treatment.

Causal
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Assertion

People with rare genetic changes that reduce ANGPTL7 gene function have lower intraocular pressure and a lower risk of developing glaucoma compared to those without these variants.

Correlational
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Assertion

In mice, removing both copies of the Angptl7 gene lowers eye pressure by about 2 mmHg, and removing one copy lowers it by 1.1 mmHg, showing that the amount of Angptl7 gene activity directly affects eye pressure levels.

Mechanistic
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Assertion

Increasing ANGPTL7 protein in mouse eyes causes intraocular pressure to rise by 2–5 mmHg within 7 days, and this protein is sufficient to elevate eye pressure in a model of glaucoma.

Causal
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Assertion

ANGPTL7 protein is found at high levels in the eye tissues that control fluid drainage, and its levels rise when corticosteroids or TGF-beta are present. These substances are known to increase eye pressure, and ANGPTL7 is part of the biological process that affects how fluid leaves the eye.

Mechanistic
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