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Disrupting this pathway—either by severing kidney sensory nerves, selectively deleting the angiotensin II type 1a receptor (AT1a) in the subfornical organ (SFO), or using optogenetics to silence the kidney-SFO or SFO-paraventricular nucleus (PVN) connections—reduces sympathetic output, which in turn diminishes structural damage and functional impairment in the kidneys and heart in these models of CKD and heart failure (Cao et al., 2023)
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