In recent years, the efficacy of electroacupuncture (EA) pretreatment generating ischemic tolerance mimicking ischemic pretreatment (IP) has been continuously confirmed, which was first found in the brain and then in the heart. Furthermore, researchers have observed the intensive cardioprotection impact of EA pretreatment on patients undergoing percutaneous coronary intervention (PCI) and heart valve replacement, indicating that EA pretreatment tends to be a valuable and advantageous avenue for preventing acute myocardial ischemia/reperfusion (I/R) injury or treatment of ischemic heart disease (IHD). In reality, the heart protection mechanism of EA pretreatment is robust and pleiotropic, of which the regulatory molecular pathways are involved in multichannel, multilevel, and multitarget, including energy metabolism, inflammatory response, calcium overload, oxidative stress, autophagy, and apoptosis. Through a growing number of clinical tests and basic experiments with animal models, researchers progressively explored the optimal acupoints and parameters, where EA pretreatment induced acute and delayed ischemic tolerance for myocardial protection. Thereby, this article aims to collect the relevant evidence on EA pretreatment against myocardial ischemia/reperfusion injury (MIRI) and summarize the mechanism of cardioprotection of EA pretreatment to provide ideas and methods for further clinical applications.

Stroke is the leading cause of long-term disability in developed countries. Multitudinous evidence suggests that treadmill training treatment is beneficial for balance and stroke rehabilitation; however, the need for stroke therapy remains unmet. In the present study, a cerebral ischemia rat model was established by permanent middle cerebral artery occlusion (pMCAO) to explore the therapeutic effect and mechanism of scalp acupuncture combined with treadmill training on ischemic stroke. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling and neuronal nuclear protein (NeuN) double staining and cellular inhibitor of apoptosis protein-1 (cIAP1) and NeuN immunofluorescence double staining were used to detect the short-term and long-term neuroprotective effects of scalp acupuncture combined with treadmill training on pMCAO rats. In addition, the antiapoptotic effect of the combined treatment was evaluated in pMCAO rats transfected with cIAP1 shRNA. Western blotting was used to detect the relative protein expression in the caspase-8/-9/-3 activation pathway downstream of cIAP1 to further clarify its regulatory mechanism. Our results showed that scalp acupuncture combined with treadmill training successfully achieved short-term and long-term functional improvement within 14 days after stroke, significantly inhibited neuronal apoptosis, and upregulated the expression of cIAP1 protein in the ischemic penumbra area of the ischemic brain. However, no significant functional improvement and antiapoptotic effect were found in pMCAO rats transfected with cIAP1 shRNA. Western blotting results showed that the combined therapy markedly inhibited the activation of the caspase-8/-9/-3 pathway. These findings indicate that scalp acupuncture combined with treadmill training therapy may serve as a more effective alternative modality in the treatment of ischemic stroke, playing an antiapoptotic role by upregulating the expression of cIAP1 and inhibiting the activation of the caspase-8/-9/-3 pathway.

Stroke-Heart Syndrome describes cardiac dysfunction following acute cerebrovascular events, with injury to the central autonomic network being a key pathological mechanism. The insular cortex and limbic system act as central hubs for neuro-cardiac regulation, integrating autonomic, neuroendocrine, and immune signals. This review summarizes the structural and functional organization of the central autonomic network, emphasizing the insula’s subregional specialization and its hemispheric bias in autonomic regulation. Generally, the right insula is more often linked to sympathetic predominance and the left to parasympathetic modulation, though this pattern is not absolute but rather contingent on subregional and methodological factors. Clinical and experimental evidence links lesions in the insula and limbic system to arrhythmias, QT interval prolongation, and myocardial injury through autonomic imbalance. Advances in neuroimaging, such as functional magnetic resonance imaging and diffusion tensor imaging, provide novel biomarkers for early cardiac risk stratification after stroke. Furthermore, emerging interventions including heart rate variability biofeedback and non-invasive vagus nerve stimulation show therapeutic potential by targeting these central circuits. Elucidating the mechanisms of central autonomic network injury, particularly involving the insula and limbic system, is essential for improving risk assessment and developing targeted therapies for Stroke-Heart Syndrome.

The pathological course of myocardial infarction (MI) entails a complex interplay between innate and adaptive immunity. Although innate immunity plays a dominant role in the tissue damage and clearance during the acute phase, recent studies have shown that T cells also play an important role in myocardial injury and remodeling. Advances in detection technologies have enabled the identification of several autoantigens and clarified the mechanistic roles of distinct T-cell subsets (such as regulatory T cells, helper T cells, cytotoxic T cells, and γδ T cells) during the remodeling phase. These T cell subsets are widely involved in myocardial inflammation, apoptosis and myocardial fibrosis, and play an important role in myocardial remodeling. This review synthesizes current progress on the repertoire of autoantigens recognized after MI, the mechanistic underpinnings of T-cell responses in myocardial remodeling, and emerging immunotherapeutic strategies aimed at mitigating adverse remodeling. Together, these insights provide a conceptual framework to guide future research and therapeutic development in this field.

Stroke remains the second leading cause of death and the third leading cause of death and disability. With the growing incidence of strokes, the incidence of post-stroke cognitive impairment (PSCI) among patients is on a steady rise. These patients commonly present with impairments in memory, attention, executive function, comprehension, and judgment, substantially affecting their everyday lives. Magnetic resonance image (MRI) and cognitive assessment scales are widely employed as diagnostic tools for PSCI. They also have notable limitations. Furthermore, cerebrospinal fluid collection is relatively complex. Growing evidence suggests that blood-based biomarkers are closely involved in the onset and progression of PSCI, as bioassay techniques and equipment have become increasingly popular and optimized. Therefore, blood-based biomarkers play an essential role in the pathogenesis and progression of PSCI. This review concentrates on the research progress of blood-based biomarkers in PSCI to explore their significance for disease identification, with the aim of offering novel insights into the clinical diagnosis and therapy of PSCI.