PERSPECTIVE Protein kinase C inhibition and diabetic retinopathy: a shot in the dark at translational research

Accepted for publication 26 June 2003 . . . . . . . . . . . . . . . . . . . . . . . R educing the incidence and slowing the progression of diabetes related microvascular complications remains a difficult challenge. In the case of diabetic retinopathy, tight glucose and blood pressure control are difficult to achieve and maintain in practice, yet still only provide partial protection against sight threatening complications in the lifetime of a person with diabetes. More than 250 000 patients every year develop sight threatening diabetic retinopathy in the United States alone, often despite good compliance with antidiabetic and antihypertensive treatments. Furthermore, the morbidity and healthcare costs associated with diabetic retinopathy are likely to escalate as the prevalence of type 2 diabetes increases and as patients with diabetes live longer. For example, the effectiveness of cholesterol lowering drugs and angiotensin converting enzyme (ACE) inhibitors in preventing macrovascular (mostly coronary heart disease) deaths, as well as the wider use of renal replacement therapy, means that patients with diabetes related complications are more likely to survive to experience the distress of failing visual acuity as a result of retinopathy. Thus, as well as improving systems for eye screening and detection of retinopathy, new therapeutic strategies are urgently needed as an adjunct to existing treatments—glucose and blood pressure reduction, photocoagulation and vitreous surgical techniques—to improve visual outcomes for patients with diabetes.