Sympathetic overactivation and catecholamine toxicity: mechanisms and therapeutic strategies for neurogenic heart injury following acute ischemic stroke

Figures

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  Figure 1. Schematic diagram of SNS activation and cardiac damage after AIS. Ischemic injury to MPFC, ACC, insular cortex, amygdala, hypothalamus, PAG, PBN, NTS, NA, and VLM is a key factor for SNS activation after AIS. After AIS, neuroinflammation and oxidative stress interweave with each other, jointly act and continuously activate the SNS, thereby leading to a sharp increase in catecholamine levels. Ultimately, it causes a series of cardiac damages such as arrhythmia, elevated troponin, cardiac dysfunction and HF. MPFC, medial prefrontal cortex; ACC, anterior cingulate cortex; PAG, periaqueductal gray; PBN, parabrachial nucleus; NTS, nucleus tractus solitarius; NA, nucleus ambiguus (NA); VLM, ventral lateral medulla; TNF-α, tumor necrosis factor-α; IL-1β, interleukin-1β; IL-6, interleukin-6; NOX, NADPH oxidase; COX, cyclooxygenase; XO, Xanthine oxidase; NOS, nitric oxide synthase; ROS, reactive oxygen species; RNS, Reactive Nitrogen Species. The figure was constructed with Figdraw (https://www.figdraw.com).

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  Figure 2. The SNS governing cardiac activity. Cardiac activity is jointly regulated by CSN and PSN, with the RVLM serving as a critical hub for cardiovascular control. MPFC, medial prefrontal cortex; ACC, anterior cingulate cortex; RVLM, rostral ventral lateral medulla; PVN, paraventricular nucleus. The figure was constructed with Microsoft PowerPoint.

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  Figure 3. The mechanism of catecholamine-triggered cardiotoxicity after AIS. After AIS, sympathetic nerve tension increases, and sustained overexcitation of the sympathetic nerve network leads to substantial catecholamine release. The activation of AR, inflammatory response, oxidative stress, Ca2+ overload and mitochondrial dysfunction constitute the main network of catecholamine-induced cardiac injury. These pathological processes are interrelated. Centered on oxidative stress, they form a complex network through multiple signaling pathways, eventually leading to cardiomyocyte apoptosis, myocardial hypertrophy and cardiac fibrosis. The relevant signal pathways or key molecules are marked below each topic in the text box. The figure was constructed with Microsoft PowerPoint.