Jennifer K. Sun

Dr. Jennifer K. Sun


Research Focus & Metrics

Academic Career Length

32Years (1995-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 June 2010 in Ophthalmology
Verified
Journal Article
Closed access
MEMichael J. Elman
Michael J. Elman
LALloyd Paul Aiello
Lloyd Paul Aiello
RBRoy W. Beck
Roy W. Beck
NBNeil M. Bressler
Neil M. Bressler
SBSusan B. Bressler
Susan B. Bressler
JSJennifer K. Sun
Jennifer K. Sun

20 July 2017 in JCI Insight
Verified
Journal Article
Open access
PDF file
EDElia J. Duh
Elia J. Duh
JSJennifer K. Sun
Jennifer K. Sun
Alan W StittAlan W Stitt
Alan W Stitt
Diabetic retinopathy (DR) causes significant visual loss on a global scale. Treatments for the vision-threatening complications of diabetic macular edema (DME) and proliferative diabetic retinopathy (PDR) have greatly improved over the past decade. However, additional therapeutic options are needed that take into account pathology associated with vascular, glial, and neuronal components of the diabetic retina. Recent work indicates that diabetes markedly impacts the retinal neurovascular unit and its interdependent vascular, neuronal, glial, and immune cells. This knowledge is leading to identification of new targets and therapeutic strategies for preventing or reversing retinal neuronal dysfunction, vascular leakage, ischemia, and pathologic angiogenesis. These advances, together with approaches embracing the potential of preventative or regenerative medicine, could provide the means to better manage DR, including treatment at earlier stages and more precise tailoring of treatments based on individual patient variations.

13 February 2017 in Diabetes Care
Verified
Journal Article
Open access
PDF file
SSSharon D. Solomon
Sharon D. Solomon
ECEmily Chew
Emily Chew
EDElia J. Duh
Elia J. Duh
LSLucia Sobrin
Lucia Sobrin
JSJennifer K. Sun
Jennifer K. Sun
TGThomas Gardner
Thomas Gardner
Diabetic retinopathy diagnostic assessment and treatment options have improved dramatically since the 2002 American Diabetes Association Position Statement (1). These improvements include the widespread adoption of optical coherence tomography to assess retinal thickness and intraretinal pathology and wide-field fundus photography to reveal clinically silent microvascular lesions. Treatment of diabetic macular edema is now achieved by intravitreous injection of anti–vascular endothelial growth factor agents, and the same drugs are now used for proliferative diabetic retinopathy. Improvements in medications and devices for the systemic therapy of diabetes have also improved the ability of patients to optimize their metabolic control. This Position Statement incorporates these recent developments for the use of physicians and patients. Diabetic retinopathy is a highly specific neurovascular complication of both type 1 and type 2 diabetes, the prevalence of which strongly correlates to both the duration of diabetes and level of glycemic control. A pooled meta-analysis involving 35 studies conducted worldwide from 1980 to 2008 estimated global prevalence of any diabetic retinopathy and proliferative diabetic retinopathy (PDR) among patients to be 35.4% and 7.5%, respectively (2). Diabetic retinopathy is the most frequent cause of new cases of blindness among adults aged 20–74 years in developed countries. Glaucoma, cataracts, and other disorders of the eye occur earlier and more frequently in people with diabetes. In addition to diabetes duration, factors that increase the risk of or are associated with retinopathy include chronic hyperglycemia (3,4), nephropathy (5), hypertension (6), and dyslipidemia (7). Intensive diabetes management with the goal of achieving near-normoglycemia has been shown in large prospective randomized studies to prevent and/or delay the onset and progression of diabetic retinopathy (8,9). Lowering blood pressure has been shown to decrease retinopathy progression in people with type 2 diabetes, although tight targets (systolic blood pressure <120 mmHg) do …

1 October 2018 in Ophthalmology
Verified
Journal Article
Closed access
TWTien Yin Wong
Tien Yin Wong
JSJennifer K. Sun
Jennifer K. Sun
RKRyo Kawasaki
Ryo Kawasaki
PRPaisan Ruamviboonsuk
Paisan Ruamviboonsuk
NGNeeru Gupta
Neeru Gupta
HTHugh R. Taylor
Hugh R. Taylor

24 November 2015 in JAMA
Verified
Journal Article
Open access
PDF file
WNWriting Committee for the Diabetic Retinopathy Clinical Research Network
Writing Committee for the Diabetic Retinopathy Clinical Research Network
JGJeffrey G. Gross
Jeffrey G. Gross
AGAdam R. Glassman
Adam R. Glassman
LJLee M. Jampol
Lee M. Jampol
SISeidu Inusah
Seidu Inusah
RBRoy W. Beck
Roy W. Beck
Proliferative diabetic retinopathy (PDR) is a leading cause of vision loss in patients with diabetes mellitus,1,2 resulting in 12 000 to 24 000 new cases of blindness each year in the United States.3 Without treatment, nearly 50% of patients with high-risk PDR experience severe vision loss within 5 years.4

1 November 2014 in JAMA Ophthalmology
Verified
Journal Article
Open access
PDF file
JSJennifer K. Sun
Jennifer K. Sun
MLMichael Lin
Michael Lin
JLJan Lammer
Jan Lammer
SPSonja Prager
Sonja Prager
RSRutuparna Sarangi
Rutuparna Sarangi
LALloyd Paul Aiello
Lloyd Paul Aiello
Diabetic macular edema (DME) is a sight-threatening manifestation of diabetic retinopathy, affecting almost 30% of individuals with more than 20 years of diabetes mellitus.1 Standard treatment for DME involves repetitive, invasive intraocular injections, which place heavy burdens on the patient, physician, and health care reimbursement. No reliable methods exist to determine which individuals with DME will gain or lose vision over time, making such predictive biomarkers a major unmet need.2 These tools would substantively enhance patient counseling, improve risk stratification, advance clinical management, and influence selection of eyes for clinical studies targeting DME.