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Significant changes in ANS activity occur during wake-to-sleep transition maintaining the adequate cardiorespiratory regulation and brain activity. Since sleep is a complex homeostatic function, partly regulated by the ANS, it is not surprising that sleep disruption trigger and\/or evidence symptoms of ANS impairment. Indeed, several studies suggest a bidirectional relationship between impaired ANS function (i.e. enhanced sympathetic drive), and the emergence\/development of sleep disorders. Furthermore, several epidemiological studies described a strong association between sympathetic-mediated diseases and the development and maintenance of sleep disorders resulting in a vicious cycle with adverse outcomes and increased mortality risk. However, which and how the sleep\/wake control and ANS circuitry becomes affected during the progression of ANS-related diseases remains poorly understood. Thus, understanding the physiological mechanisms underpinning sleep\/wake-dependent sympathetic modulation could provide insights into diseases involving autonomic dysfunction. The purpose of this review is to explore potential neural mechanisms involved in both the onset\/maintenance of sympathetic-mediated diseases (Rett syndrome, congenital central hypoventilation syndrome, obstructive sleep apnoea, type 2 diabetes, obesity, heart failure, hypertension, and neurodegenerative diseases) and their plausible contribution to the generation of sleep disorders in order to review evidence that may serve to establish a causal link between sleep disorders and heightened sympathetic activity.<\/jats:p>","DOI":"10.1093\/sleep\/zsac166","type":"journal-article","created":{"date-parts":[[2022,7,25]],"date-time":"2022-07-25T23:08:39Z","timestamp":1658790519000},"source":"Crossref","is-referenced-by-count":21,"title":["Sleep dysregulation in sympathetic-mediated diseases: implications for disease progression"],"prefix":"10.1093","volume":"45","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0109-0672","authenticated-orcid":false,"given":"Mar\u00eda 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