Sleep Disturbance and Cardiometabolic Risk: Neural Control, Adipose Immunometabolism, and Vascular Injury

Sleep disturbance - obstructive sleep apnea (OSA), sleep fragmentation, short sleep duration, circadian misalignment, and insomnia - is consistently associated with cardiometabolic disease, and controlled sleep restriction and misalignment studies in humans and rodents establish causal effects on glucose regulation, adipose function, and vascular tone. What remains unresolved is mechanism: how distinct forms of sleep disruption converge on, or diverge in, the pathways that produce tissue-level metabolic and vascular injury.Adipose tissue is a metabolic and immunological organ that responds to intermittent hypoxia and fragmented sleep with insulin resistance, altered adipokine secretion, immune-cell remodeling, and low-grade systemic inflammation. These peripheral changes are not autonomous. The hypothalamic and brainstem circuits that generate sleep and set circadian phase also govern sympathetic outflow to adipose depots, vasculature, and the adrenal medulla, and neuroendocrine output on the same timescale. Chronic sympathetic overactivation and blunted baroreflex sensitivity are therefore both consequences of disrupted central regulation and drivers of endothelial dysfunction and arterial stiffening - placing the brain upstream of the peripheral cascade rather than alongside it.This Research Topic seeks work that connects central regulation to peripheral outcome across the full range of sleep disturbances, in order to identify high-risk clinical phenotypes and inform targeted therapy.We welcome Original Research, Reviews, and other article types addressing, but not limited to:● Hypothalamic, brainstem, and circadian circuits linking sleep and sleep loss to sympathetic outflow, neuroendocrine output, and peripheral metabolic control● Adipose tissue insulin resistance, adipokine signaling (leptin, adiponectin), and immune-cell remodeling following sleep fragmentation, intermittent hypoxia, or circadian misalignment● Systemic inflammation and immune-metabolic cross-talk: circulating mediators, tissue-resident immunity, and their dependence on the form and duration of sleep disruption● Autonomic phenotyping in humans (muscle sympathetic nerve activity, baroreflex sensitivity, heart-rate variability) as a mediator of metabolic and vascular injury across OSA, short sleep, insomnia, and shift work● Endothelial dysfunction and arterial stiffening arising from combined metabolic and autonomic stress● Comparative and mechanistic studies distinguishing effects specific to intermittent hypoxia from those common to sleep loss more generally● Behavioral, nutritional, exercise, device-based, and pharmacological interventions - including incretin-based therapies - evaluated against metabolic, autonomic, and vascular endpoints Topic editors: Prachi Singh, Camila Paixão Jordão Source: https://www.frontiersin.org/research-topics/85751/sleep-disturbance-and-cardiometabolic-risk-neural-control-adipose-immunometabolism-and-vascular-injury