Artificial intelligence applied in cardiovascular disease: a bibliometric and visual analysis.

Background: With the rapid development of technology, artificial intelligence (AI) has been widely used in the diagnosis and prognosis prediction of a variety of diseases, including cardiovascular disease. Facts have proved that AI has broad application prospects in rapid and accurate diagnosis. Objective: This study mainly summarizes the research on the application of AI in the field of cardiovascular disease through bibliometric analysis and explores possible future research hotpots. Methods: The articles and reviews regarding application of AI in cardiovascular disease between 2000 and 2023 were selected from Web of Science Core Collection on 30 December 2023. Microsoft Excel 2019 was applied to analyze the targeted variables. VOSviewer (version 1.6.16), Citespace (version 6.2.R2), and a widely used online bibliometric platform were used to conduct co-authorship, co-citation, and co-occurrence analysis of countries, institutions, authors, references, and keywords in this field. Results: A total of 4,611 articles were selected in this study. AI-related research on cardiovascular disease increased exponentially in recent years, of which the USA was the most productive country with 1,360 publications, and had close cooperation with many countries. The most productive institutions and researchers were the Cedar sinai medical center and Acharya, Ur. However, the cooperation among most institutions or researchers was not close even if the high research outputs. Circulation is the journal with the largest number of publications in this field. The most important keywords are "classification", "diagnosis", and "risk". Meanwhile, the current research hotpots were "late gadolinium enhancement" and "carotid ultrasound". Conclusions: AI has broad application prospects in cardiovascular disease, and a growing number of scholars are devoted to AI-related research on cardiovascular disease. Cardiovascular imaging techniques and the selection of appropriate algorithms represent the most extensively studied areas, and a considerable boost in these areas is predicted in the coming years.

ASCs-EVs Inhibit Apoptosis and Promote Myocardial Function in the Infarcted Heart via miR-221.

BACKGROUND: Extracellular vehicles (EVs) secreted from adipose-derived stem cells (ASCs) (ASCs-EVs) have the potential to treat myocardial infarction (MI), although the underlying mechanism remains unclear. The current study explored the ability of ASCs-EVs to inhibit apoptosis and promote myocardial function in the infarcted heart via microRNAs (miRNAs)-221. METHODS: In hypoxia-induced H9C2 cells, a cardiac cell strain derived from the SD Rat left ventricle, we measured the cell viability and apoptosis-related protein expression after transfection with the ASCs-EVs-NC (negative control for EVs-miR-221) or ASCs-EVs-miR-221 mimics. We then verified the cardioprotective effects of miR-221-overexpressing ASCs-EVs by investigating myocardial cell apoptosis and cardiac function in a MI rat model treated with ASCs-EVs from miR-221-overexpressing ASCs by comparing control with ASC treatment. RESULTS: The in vitro experiment results showed that the proliferation of H9C2 cells and the anti-apoptotic protein expression were significantly enhanced by the ASCs-EVs-miR-221 mimic. The in vivo experiment results found that ASCs-EVs from miR-221-overexpressing ASCs have cardioprotective effects, as demonstrated by lower serum troponin levels and left ventricular end-systolic volume, and a lower number of apoptotic myocardial cells than those in control and ASC-treated rats. CONCLUSIONS: ASCs-EVs have therapeutic effects on MI by inhibiting cardiomyocyte apoptosis via miR-221.

Efficacy and safety of scalp acupuncture for poststroke depression: A meta-analysis and systematic review.

BACKGROUND: Poststroke depression (PSD) is a common clinical poststroke complication that adversely affects cognitive and physical function rehabilitation. Scalp acupuncture (SA) can significantly improve somatic dysfunction and emotional disorder in stroke patients. This meta-analysis aims to evaluate the effectiveness and safety of SA in the treatment of PSD. METHODS: We conducted a comprehensive search of multiple electronic databases, including PubMed, Cochrane Library, Embase, Web of Science, China National Knowledge Internet, China Science and Technology Journal Database, Wan Fang Data Knowledge Service Platform, and China Biology Medicine databases until December 20, 2022, to identify randomized controlled trials investigating the efficacy of SA in the treatment of PSD. Two independent researchers screened the literature, extracted data, and assessed the risk of bias in the included studies based on the inclusion and exclusion criteria. We performed a meta-analysis of the eligible literature using RevMan 5.4.1 and Stata 15.0 software. RESULTS: This study comprised a total of 14 randomized controlled trials, 10 of which used SA and 4 of which used SA in combination with electroacupuncture therapy. The results of the meta-analysis revealed that the effective rate of the SA group was significantly higher than that of the Western medicine group (relative risk = 1.09, 95% confidence interval (CI) [1.02, 1.16], P = .008). Moreover, compared to the Western medicine group, the SA group demonstrated significant improvements in Hamilton depression scale scores (mean difference = -2.29, 95% CI [-3.88, -0.70], P = .005) and neurological function deficit scores (mean difference = -3.06, 95% CI [-5.91, -0.21], P = .04). Additionally, the SA group has a lower incidence of adverse events than the western medicine group (relative risk = 0.12, 95% CI [0.05, 0.29], P < .00001). CONCLUSION: SA has superior efficacy and safety compared to Western medicine for PSD. These findings suggest that SA could be a promising alternative treatment for the assessed condition. Due to the limited number and quality of the included literature, the above conclusions must be confirmed by additional high-quality research.

Anti-apoptosis effect of traditional Chinese medicine in the treatment of cerebral ischemia-reperfusion injury.

Cerebral ischemia, one of the leading causes of neurological dysfunction of brain cells, muscle dysfunction, and death, brings great harm and challenges to individual health, families, and society. Blood flow disruption causes decreased glucose and oxygen, insufficient to maintain normal brain tissue metabolism, resulting in intracellular calcium overload, oxidative stress, neurotoxicity of excitatory amino acids, and inflammation, ultimately leading to neuronal cell necrosis, apoptosis, or neurological abnormalities. This paper summarizes the specific mechanism of cell injury that apoptosis triggered by reperfusion after cerebral ischemia, the related proteins involved in apoptosis, and the experimental progress of herbal medicine treatment through searching, analyzing, and summarizing the PubMed and Web Of Science databases, which includes active ingredients of herbal medicine, prescriptions, Chinese patent medicines, and herbal extracts, providing a new target or new strategy for drug treatment, and providing a reference for future experimental directions and using them to develop suitable small molecule drugs for clinical application. With the research of anti-apoptosis as the core, it is important to find highly effective, low toxicity, safe and cheap compounds from natural plants and animals with abundant resources to prevent and treat Cerebral ischemia/reperfusion (I/R) injury (CIR) and solve human suffering. In addition, understanding and summarizing the apoptotic mechanism of cerebral ischemia-reperfusion injury, the microscopic mechanism of CIR treatment, and the cellular pathways involved will help to develop new drugs.

Lactate and Lactylation in the Brain: Current Progress and Perspectives.

As the final product of glycolysis, lactate features not only as an energy substrate, a metabolite, and a signaling molecule in a variety of diseases-such as cancer, inflammation, and sepsis-but also as a regulator of protein lactylation; this is a newly proposed epigenetic modification that is considered to be crucial for energy metabolism and signaling in brain tissues under both physiological and pathological conditions. In this review, evidence on lactylation from studies on lactate metabolism and disease has been summarized, revealing the function of lactate and its receptors in the regulation of brain function and summarizing the levels of lactylation expression in various brain diseases. Finally, the function of lactate and lactylation in the brain and the potential mechanisms of intervention in brain diseases are presented and discussed, providing optimal perspectives for future research on the role of lactylation in the brain.

Poststroke Cognitive Impairment Research Progress on Application of Brain-Computer Interface.

Brain-computer interfaces (BCIs), a new type of rehabilitation technology, pick up nerve cell signals, identify and classify their activities, and convert them into computer-recognized instructions. This technique has been widely used in the rehabilitation of stroke patients in recent years and appears to promote motor function recovery after stroke. At present, the application of BCI in poststroke cognitive impairment is increasing, which is a common complication that also affects the rehabilitation process. This paper reviews the promise and potential drawbacks of using BCI to treat poststroke cognitive impairment, providing a solid theoretical basis for the application of BCI in this area.

Effects of Shendibushen on the Expression of CD146 and its Metabolic Pathways.

Context: Evidence from multiple studies has revealed that it's meaningful to evaluate the clinical significance of CD146 because it's related to an early diagnosis of chronic renal failure as well as to the severity of illness and the patient's prognosis. Objective: The current study intended to evaluate the therapeutic effects of Shendibushen on the clinical parameters of blood and urine and on fibrosis in the kidney in a rat model, using simulated renal tissue fibrosis that was surgically induced with unilateral ureteral obstruction (UUO). Also, our research team intended to analyze the metabolic pathway activated by Shendibushen both in rat and human kidneys through use of the Kyoto Encyclopedia of Genes and Genomes (KEGG) database and the GeneNetwork. The aim is to discover if a connection existed between CD146 and key genes in these pathways. Design: The research team conducted an animal study in Wistar rats. Intervention: The rats were divided into 5 groups of 14 animals each: (1) blank control group, (2) sham control group, (3) model group, (4) Niaoduqing group, and (5) Shendibushen group. Three groups had UUO surgically induced-the model, Niaoduqing, and Shendibushen groups. The sham control group received sham surgery, and the blank control group received no surgery. The Shendibushen and Niaoduqing groups received the relevant capsules once a day at a fixed time, for a total of 28 days. Outcome Measures: The levels of serum creatinine, blood urea nitrogen, microalbuminuria, serum soluble CD146, and urinary soluble CD146 were measured on the 14th and 28th days after modeling the rats. The degree of renal interstitial fibrosis was examined by hematoxylin and eosin (HE) staining and Masson trichrome staining. The changes at transcriptome level were obtained by target tissue sequencing. The KEGG database was used to analyze the potential pathway activated by the Shendibushen treatment. The GeneNetwork analysis was used to validate the correlation and identify the connections between CD146 and the key genes of the potential pathways. Results: Shendibushen capsules decreased the degree of renal interstitial fibrosis in the UUO rat model and reduced the serum creatinine, blood urea nitrogen, microalbumin, serum sCD146, and urinary sCD146 significantly compared to the model group (P < .05). Upon analysis of the metabolic pathways activated by Shendibushen, the study further verified, through use of the KEGG database, that CD146 activated the nuclear factor kappa B1 (NF-κB1) and transforming growth factor beta 1 (TGF-ß1)/ SMAD family member 2 (SMAD2) pathways. Conclusions: CD146 could become an early indicator in clinical monitoring. CD146 has a function related to the NF-κB1and TGF-ß1/ SMAD2 pathways under Shendibushen treatment.

Acupuncture protects against cerebral ischemia-reperfusion injury via suppressing endoplasmic reticulum stress-mediated autophagy and apoptosis.

BACKGROUND: Acupuncture treatment possesses the neuroprotection potential to attenuate cerebral ischemia-reperfusion (I/R) injury. Endoplasmic reticulum (ER) stress has been suggested to be involved in the pathogenic mechanism of cerebral I/R injury. Whether acupuncture protects against cerebral I/R injury via regulating ER stress remains unclear. This study aimed to evaluate the role of ER stress in the neuroprotection of acupuncture against cerebral I/R injury and its underlying mechanisms. METHODS: Cerebral I/R injury was induced by middle cerebral artery occlusion (MCAO) in rats. Acupuncture was carried out at Baihui (GV 20), and Qubin (GB7) acupoints in rats immediately after reperfusion. The infarct volumes, neurological score, ER stress, autophagy and apoptosis were determined. RESULTS: Acupuncture treatment decreased infarct volume, neurological score and suppressed ER stress via inactivation of ATF-6, PERK, and IRE1 pathways in MCAO rats. Attributing to ER stress suppression, 4-PBA (ER stress inhibitor) promoted the beneficial effect of acupuncture against cerebral I/R injury. Whereas, ER stress activator tunicamycin significantly counteracted the neuroprotective effects of acupuncture. In addition, acupuncture restrained autophagy via regulating ER stress in MCAO rats. Finally, ER stress took part in the neuroprotective effect of acupuncture against apoptosis in cerebral I/R injury. CONCLUSIONS: Our findings suggest that acupuncture offers neuroprotection against cerebral I/R injury, which is attributed to repressing ER stress-mediated autophagy and apoptosis.

Eugenol Attenuates Cerebral Ischemia-Reperfusion Injury by Enhancing Autophagy via AMPK-mTOR-P70S6K Pathway.

Eugenol, as an active compound isolated from Acorus gramineus, has been shown to protect against cerebral ischemia-reperfusion (I/R) injury. Nonetheless, the detailed neuroprotective mechanisms of eugenol in cerebral I/R injury have not been elaborated. In the present study, cerebral I/R injury model was established by middle cerebral artery occlusion (MCAO) in rats. HT22 cells were subjected to oxygen-glucose deprivation/reperfusion (OGD/R) to mimic cerebral I/R injury in vitro. The results showed that eugenol pre-treatment relieved cerebral I/R injury as evidenced by improving neurological deficits and reducing infarct volume. Autophagy was induced by MCAO, which was further promoted by eugenol administration. Moreover, rapamycin, an activator of autophagy, promoted eugenol-induced decreases in neurological score, infarct volume, brain water content, and apoptosis. However, pretreatment with 3-MA, an inhibitor of autophagy, led to the opposite results. Similarly, eugenol pretreatment increased the viability and restrained apoptosis of OGD/R-challenged HT22 cells. OGD/R-induced autophagy was strengthened by eugenol. Mechanically, eugenol promoted autophagy through regulating AMPK/mTOR/P70S6K signaling pathway in vivo and in vitro. In conclusion, pretreatment with eugenol attenuated cerebral I/R injury by inducing autophagy via AMPK/mTOR/P70S6K signaling pathway.

Proteomics Research on the Protective Effect of Mangiferin on H9C2 Cell Injury Induced by H2O2.

Cardiovascular disease is one of the leading causes of morbidity and mortality worldwide. Mangiferin is a natural glucosylxanthone with antioxidant and anti-inflammatory properties, which has been confirmed to protect cardiac cells from myocardial infarction and myocardial ischemia reperfusion injury (MIRI); however, the underlying mechanism is still unclear. As oxidative stress is a major pathogenesis of MIRI, an H9C2 cell injury induced by hydrogen peroxide (H2O2) was established to simulate MIRI in vitro. Herein, the protective effect of mangiferin against MIRI was evaluated and the isobaric tags for relative and absolute quantitation (iTRAQ)-based proteomics was applied to explore the underlying molecular mechanism. In this research, mangiferin markedly ameliorated the oxidative imbalance by increasing the antioxidative capacity of the H9C2 cell. Moreover, proteomics analysis revealed that mangiferin pretreatment brought twenty differently-expressed proteins back to normal, most of which were related to glucose and fatty acid metabolism. Glycolysis, citrate cycle, and fatty acid degradation pathways were highlighted by Kyoto Encyclopedia of Gene and Genomes (KEGG) analysis. Western blot validation of six cardiac metabolism-related proteins were consistent with the proteomics analysis. Taken together, mangiferin protected the cardiomyocytes from MIRI by enhancing the antioxidant capacity and increasing the activities of glycolysis, citrate cycle, and fatty acid degradation pathways.