cium waves in endothelia (9). The effects on nitric oxide generation are also intriguing and strongly implicate caveolae in the regulation of nitric oxide synthases, either directly or through the control of calcium ions. Supporting these findings, a synthetic caveolin -derived peptide specifically inhibited acetylcholine-induced vasodilation and nitric oxide generation in endothelia (10). Although the Drab et al. mice generally appeared healthy, subsequent tests showed that they were physically weak and that their lungs displayed severe abnormalities, with increased cell numbers and a disorganized architecture. The causes of these abnormalities are hard to discern but are at least consistent with hyperproliferation due to loss of the normal control of cell proliferation (4). If this turns out to be the case, it is not yet clear why hyperproliferation abnormalities are found in the lungs but not in other tissues that are nor
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Cohen et al. (2001) studied this question.
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