Aging is a risk factor for cardiovascular disease, and there is no effective therapeutic approach to alleviate this condition. NF-κB and TNF-α have been implicated in the activation of the aging process, but the signaling molecules responsible for the inactivation of NF-κB and TNF-α remain unknown. Exosomes have been reported to improve heart functions by releasing miRNA. Recent studies suggest that lncRNAs are more tissue-specific and developmental stage-specific compared to miRNA. However, the role of lncRNA in exosome-mediated cardiac repair has not been explored. In the present study, we focused on metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), which is an lncRNA associated with cell senescence. We discovered that human umbilical cord mesenchymal stem cell- (UMSC-) derived exosomes prevent aging-induced cardiac dysfunction. Silencer RNA against lncRNA MALAT1 blocked the beneficial effects of exosomes. In summary, we discovered that UMSC-derived exosomes prevent aging-induced cardiac dysfunction by releasing novel lncRNA MALAT1, which in turn inhibits the NF-κB/TNF-α signaling pathway. These findings will lead to the development of therapies that delay aging and progression of age-related diseases.

The human gastrointestinal tract harbors a complex and diverse microbial community. Emerging evidence has revealed bidirectional communication between the gut microbiome and the central nervous system, termed the “microbiota–gut–brain axis”. This axis serves as a critical regulator of glial cell function, positioning it as an essential target for ameliorating the onset and progression of ischemic stroke. In this review, we discuss the developments in the relationship between ischemic stroke and neuroinflammation via MGBA. The gut microbiome plays a critical role in signaling to microglia, astrocytes, and other immune components within this axis. We also summarize the interactions between the gut microbiota and glial cells under both healthy and ischemic stroke conditions. Additionally, we also focus on the role of microbiota-derived metabolites and neurotransmitters in ischemic stroke. Furthermore, we investigate the potential of targeting the intestinal and blood–brain barriers to improve MGBA. Finally, we evaluate the preclinical and clinical evidence for dietary interventions, probiotics, prebiotics, and fecal microbiota transplantation in ischemic stroke. A comprehensive understanding of the MGBA is essential for developing MGBA-based treatment for ischemic stroke.

The neutrophil-to-lymphocyte ratio (NLR), an inflammatory marker, plays an important role in the inflammatory mechanisms of the pathophysiology and progression of acute ischemic stroke (AIS). The aim of this study was to identify the potential factors associated with functional prognosis in AIS. A total of 303 AIS patients were enrolled in this study; baseline information of each participant, including demographic characteristics, medical history, laboratory data, and 90-day functional outcome, was collected. Multivariate logistic regression analysis revealed that NLR, systolic blood pressure (SBP) and National Institutes of Health Stroke Scale (NIHSS) score were found to be independent factors for poor functional outcomes. Receiver operating characteristic (ROC) curve analysis was performed to estimate the predictive value of the NLR for 90-day functional outcome, with the best predictive cutoff value being 3.06. In the multivariate logistic regression analysis, three models were constructed: Model 1, adjusted for age, sex, SBP, and TOAST classification (AUC = 0.694); Model 2, further adjusted for the NIHSS score at admission (AUC = 0.826); and Model 3, additionally adjusted for the NLR (AUC = 0.829). The NLR at admission was an independent predictor of 90-day prognosis in patients with AIS. The risk factors related to poor 90-day functional outcomes were higher SBP, higher NLR, and a greater NIHSS score.

Post-stroke cognitive impairment (PSCI) is a significant neurological complication, affecting up to one-third of stroke survivors. Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia, significantly increasing the risk of ischemic stroke. Increasing evidence suggests that AF plays a pivotal role in exacerbating cognitive decline in stroke patients. This review integrates current clinical, imaging, and mechanistic findings to elucidate how AF-related strokes exacerbate cognitive decline through multiple overlapping pathways, including thromboembolism, neuroinflammation, atherosclerosis, cerebral hypoperfusion, cerebral small vessel disease, and silent infarctions. These processes collectively impair cerebrovascular integrity, induce neuronal damage, and accelerate brain aging. The review further evaluates the role of clinical and neuroimaging biomarkers as predictive tools and their utility in guiding therapeutic strategies. By integrating insights of the latest researches, we aim to provide a comprehensive framework for alleviating cognitive decline in patients with AF-related stroke and highlight future research directions.

Post-stroke cognitive impairment (PSCI) is a common and severe complication of stroke, significantly reducing patients' quality of life and life expectancy while imposing a heavy burden on families and society. MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression at the post-transcriptional level and play critical roles in the development, plasticity, and repair of the central nervous system. Recent studies have revealed that multiple miRNAs are aberrantly expressed after cerebral ischemia and contribute to PSCI progression by modulating key processes such as oxidative stress，cell death，neuroinflammation, blood-brain barrier，myelin repair. This review summarizes recent advances in understanding the roles, target genes, and signaling pathways of miRNAs in PSCI, and discusses their potential as early diagnostic biomarkers and therapeutic targets, aiming to provide a theoretical basis and research direction for the precision management of PSCI.

Background: Post-stroke depression (PSD) is a common complication of stroke, which seriously affects the functional outcome of patients. Systemic low-grade inflammation associated with PSD has been shown to occur at several months to years, however, whether these inflammatory markers predicted PSD at an acute stage of stroke is controversial. Method: A total of 625 patients with acute ischemic stroke (219 female, 35.40%) were included in this study. PSD was diagnosed using the 17-item Hamilton depression scale (HAMD) at 7 days following discharge (7–14 days after stroke onset). Multivariable logistic regression analysis was applied to build a prediction model for PSD at discharge. Discrimination and calibration of the model were assessed by C-index, calibration plot. Internal validation was conducted using bootstrapping validation. Results: At discharge of hospitalization, 95 patients (15.20%) were diagnosed with PSD. Multivariable logistic regression suggested that female gender (OR = 2.043, 95% CI = 1.287–3.245, p = 0.002), baseline NIHSS (OR = 1.108, 95% CI = 1.055–1.165, p < 0.001) and fibrinogen (OR = 1.388, 95% CI = 1.129–1.706, p = 0.002) were independent predictors for PSD at discharge. The cut-off of the fibrinogen plasma level was 3.08 g/L. These predictors were included in the nomogram. The model displayed good discrimination, with a C-index of 0.730 (95% CI = 0.683–0.777) and good calibration. Conclusion: Female gender, baseline stroke severity and a higher level of fibrinogen were independently associated with PSD at discharge. A nomogram based on these three predictors can be used to provide an individual, visual prediction of the risk probability of PSD.