advertisement
The publication of Pang et al. (88) presents laboratory data and comes to the conclusion that inducible nitric oxide synthase (NOS-2, iNOS) is not responsible for the optic neuropathy in glaucoma. Nevertheless, there is a significant literature using a variety of techniques that supports the hypothesis that excessive NO, made by NOS-2 in astrocytes of the optic nerve head, is damaging to the axons of the retinal ganglion cells in glaucoma.2 Compared to previous reports that studied NOS-2 in glaucoma, Pang et al. used a different rat model, an ambiguous method to measure exposure to elevated IOP, a semi-quantitative method to assess retinal ganglion cell loss and other differences from reported methods. Whereas the authors' conclusion may be correct for the experiments that they performed, the authors have made a generalized, overstated, conclusion based on their assumptions that all animal models and all methods must give the same answer. In fact, the underlying mechanisms in different models need not be similar and all methods are not equivalent. Indeed, not all glaucoma patients are the same:
The investigators collaborating in Pang et al. have published numerous papers, but have not put forth a mechanism for glaucomatous optic neuropathy and retinal ganglion cell death. Workers in the field look forward to seeing these investigators use their considerable technical resources to discover a viable mechanism that may be of use for treating glaucoma patients. After all, why else are we doing research?