Introduction by Tony Realini, MD, MPH, section editor
This issue of Glaucoma Today features a new regular column, the “Clinician Scientist's Corner.” The glaucoma community is rich with physicians who are busy clinically but also devote a significant proportion of their professional time to research activities. Many of the pillars of the glaucoma community are clinician scientists, and GToday regularly profiles these established individuals in the “5 Questions” column. During the past few decades, however, there was something of a dropoff in the number of academic glaucoma specialists who were dually active in clinical care and research. Perhaps this was a consequence of economics. Because reimbursements for clinical services continue to dwindle, it is no longer possible to subsidize 1 or 2 days of academic activity by seeing patients 3 or 4 days a week. Moreover, extramural funding to support research time and costs became harder to obtain; indeed, the climate for National Institutes of Health funding may never have been as harsh as recently due to the economic recession.
Fortunately for the glaucoma community, and more importantly for patients, the number of early- and midcareer clinician scientists in glaucoma is growing again. Many academic institutions are adapting to the changing paradigm for research funding and are investing in protected time and startup costs for young researchers. The National Institutes of Health also deserve credit for establishing and generously funding a line of career development grants for clinicians aspiring to both basic and clinical research. Other organizations such as the American Glaucoma Society and Research to Prevent Blindness also offer grants to clinician scientists, with award amounts that are sufficient to support meaningful research programs. Once seemingly headed for extinction, the glaucoma clinician scientist seems again to be alive and well.
As section editor, my goal for this column is to provide early- and midcareer glaucoma clinician scientists with a forum to showcase their active research programs. What are they working on? Where are they in the process? What impact will their work have on patients' care? I will also task contributors with describing the evolution of their careers from clinician to clinician scientist. What drew them to research? How do they integrate patients' care and their research activities? How do they support their research efforts?
I hope that this column will both educate and inspire readers. Glaucoma specialists in the trenches with burgeoning clinical practices may find comfort in knowing that the common clinical conundrums they face every day are the topic of someone's research program and that evidence-based guidance may be just around the corner. This column will also introduce young residents and glaucoma fellows to their peers who are succeeding in the dual life of clinician and scientist and, in so doing, may encourage them to follow similar dreams. Everyone needs role models.
I hope you find value in this new column, and I welcome your feedback.
It is an honor to be profiled in the inaugural
installment of the “Clinician
Scientist's Corner” column and to discuss
my research.
MOTIVATION
I pursue scientific research in addition
to clinical practice so that I may investigate
the underlying mechanisms of glaucoma. I believe
in the adage, “Through clinical care, you can help individuals
in a personal and possibly profound way, while
through research, you have the potential to help populations
of people.” I would not have been able to pursue
both clinical care and research without the mentorship
and support that I received along the way.
FOCUS
I investigate the molecular biology of the trabecular
meshwork, which has direct relevance for clinical glaucoma.
It seems more the rule than the exception that
glaucoma patients require progressively more IOPlowering
interventions over time. The likely reason is
that current treatments are palliative: they may lower
the IOP, but they do not interrupt the dysfunctional
processes that cause the IOP to rise. Previous excellent
work has shown that homeostasis of the extracellular matrix in the trabecular meshwork is involved in the
regulation of IOP and that dysregulation of the extracellular
matrix is part of the pathophysiology of ocular
hypertension.1,2
In the laboratory, my colleagues and I work to elucidate the molecular mechanisms of the extracellular matrix's synthesis and degradation. We published evidence that matricellular proteins—particularly SPARC (secreted protein acidic and rich in cysteine)—are involved in the regulation of IOP, probably by affecting the extracellular matrix's synthesis.3 We have additional information on the mechanistic regulation of SPARC, which we hope to publish soon.
Other groups have demonstrated that prostaglandin analogues exert a regulatory influence on matrix metalloproteinases and tissue inhibitors of metalloproteinases in the ciliary body.4-6 We have built on this finding and shown that variable effects of prostaglandin analogues on matrix metalloproteinases and tissue inhibitors of metalloproteinases in the trabecular meshwork and ciliary body may mechanistically explain the observations of enhanced outflow through both trabecular and uveoscleral pathways as well as the differential effectiveness of the prostaglandin analogues.
It is my hope that our work will lead to an understanding of the pathophysiologic process by which dysfunction in the trabecular meshwork begins. This information may provide new therapeutic targets for drug delivery so that clinicians may more directly intervene in the glaucomatous process.
Section Editor Tony Realini, MD, MPH, is an associate professor of ophthalmology at West Virginia University Eye Institute in Morgantown. Dr. Realini may be reached at (304) 598- 6884; realinia@wvuh.com.
Douglas J. Rhee, MD, is an assistant professor of ophthalmology at the Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston. Dr. Rhee may be reached at (617) 573-3670; douglas_rhee@meei.harvard.edu.
