Scutellarin (SCU), a flavonoid glucuronide derived from Scutellaria barbata and Erigeron breviscapus, exhibits broad pharmacological effects with promising therapeutic potential in treating various chronic diseases. It has demonstrated efficacy in modulating multiple biological pathways, including antioxidant, anti-inflammatory, anti-apoptotic, and vasodilatory mechanisms. These protective roles make SCU a valuable compound in treating chronic diseases such as cerebrovascular diseases, cardiovascular diseases, neurodegenerative disorders, and metabolic diseases. Despite its multi-targeted effects, SCU faces challenges such as low bioavailability and limited clinical data, which hinder its widespread therapeutic application. Current research supports its potential to prevent oxidative stress, reduce inflammatory responses, and enhance cell survival in cells and rats. However, more comprehensive studies are required to clarify its molecular mechanisms and to develop strategies that enhance its bioavailability for clinical use. SCU could emerge as a potent therapeutic agent for the treatment of chronic diseases with complex pathophysiological mechanisms. This review examines the current literature on Scutellarin to provide a comprehensive understanding of its pharmacological activity, mechanisms of action, and therapeutic potential in treating chronic diseases.

Objective: Suicide resilience is gaining increasing attention from researchers because of its potential role in preventing suicide. However, it has not been clearly analyzed, and there are various meanings and terms regarding this issue. The purpose of this analysis, therefore, was to conceptualize the concept of suicide resilience.Methods: Walker and Avant's method of concept analysis was used to identify the antecedents, attributes, and consequences of suicide resilience. The literature was searched using PubMed, PsychINFO, Embase, Web of Science, CINAHL, CNKI, and WanFang databases with no limitation on publication date. The search included peer-reviewed journal articles and dissertations related to suicide resilience published in English or Chinese.Results: 52 articles were identified to provide information for this concept analysis. Five defining attributes of suicide resilience were identified: social support, coping strategies, psychological capital, meaning in life, and sense of responsibility. Antecedents of suicide resilience were high suicide risk events, and consequences of suicide resilience were keeping vulnerable individuals stay away from or overcoming suicidality.Conclusions: The result of the analysis provided a more clear definition of suicide resilience. The identified defining attributes, antecedents, and consequences can be further tested and used to develop potential interventions. Future research is needed and will help to advance our understanding of the scope.

Systemic lupus erythematosus (SLE) is a prevalent autoimmune disease primarily characterized by the involvement of multiple systems and organs. Cardiovascular disease is the primary cause of mortality in patients with SLE, though the mechanisms underlying the increased cardiovascular risk in SLE patients remain unclear. Recent studies indicate that abnormal activation of programmed cell death (PCD) signaling and the crosstalk among various forms of cell death are critical in the immunopathogenesis of SLE. Furthermore, apoptosis, necroptosis, pyroptosis, NETosis, and ferroptosis are recognized as key cellular processes in the pathogenesis of SLE and are closely linked to cardiac involvement. This review uniquely explores the intricate crosstalk between apoptosis, necroptosis, and other cell death pathways, discussing their roles and interactions in the pathogenesis of cardiac involvement in SLE. Investigating the interplay between PCD signaling and cardiac involvement in SLE in understanding the disease’s underlying mechanisms and offers opportunities for new therapeutic interventions. The integration of precision medicine and innovative strategies targeting these complex pathways holds promise for enhancing the treatment prospects of SLE with cardiac involvement.

Heart failure (HF) represents the terminal stage of various cardiovascular diseases, with current treatment options remaining limited. Shenfuyixin Granules (SFYX) have been integrated into clinical practice, demonstrating significant therapeutic efficacy. However, the underlying mechanisms of action are still not fully understood. This study aims to investigate whether SFYX promotes mitochondrial autophagy and enhances cardiac function in HF following myocardial infarction via the SIRT3/FOXO1 signaling axis. The rat model of HF was established by ligation of the left anterior descending artery, while in vitro experiments were conducted using H9C2 cells. The blood-entry components of SFYX were identified using ultra-high-performance liquid chromatography coupled with tandem mass spectrometry (UPLC-MS/MS). Network analysis, integrating proteomics and transcriptomics, was conducted to determine the active components of SFYX and elucidate the key regulatory mechanisms involved in its treatment of HF. After a 4-week intervention with SFYX, cardiac function was assessed via echocardiography. Myocardial infarct size was measured using triphenyl tetrazolium chloride (TTC) staining, while H&E and Masson staining were employed to evaluate myocardial tissue fibrosis and hypertrophy. Mitochondrial function was assessed using transmission electron microscopy and JC-1 dye. Cell apoptosis was detected via TUNEL assay. Additionally, molecular docking was performed to assess the binding affinity between key components of SFYX and autophagy-related proteins. Mechanistically, the expression levels of SIRT3, FOXO1, P62, and BNIP3 were determined using quantitative PCR and Western blotting. UPLC-MS/MS analysis revealed 21 blood-entry components in SFYX. Integrated analyses of network pharmacology, proteomics, and transcriptomics indicated that SFYX may ameliorate HF by stimulating mitochondrial autophagy through activation of the SIRT3/FOXO1 pathway. Compared with the model group, SFYX significantly attenuated myocardial hypertrophy, apoptosis, and fibrosis while enhancing autophagy, which may be partially attributed to the recovery of mitochondrial function. We propose that SFYX enhances mitochondrial function by reducing membrane potential and reactive oxygen species (ROS) production. Further results demonstrated that SFYX treatment upregulated SIRT3 and FOXO1 levels while inhibiting FOXO1 acetylation. Furthermore, the levels of mitophagy-associated proteins (ATG5, ATG7, BNIP3, and LC3B-II), which are downstream mediators of FOXO1, were enhanced by SFYX. Activation of SIRT3 or overexpression of FOXO1 enhanced the cardioprotective efficacy of SFYX, whereas inhibition of SIRT3 or silencing of FOXO1 partially reversed SFYX-induced favorable activities. Molecular docking analysis revealed that Glyceryl linolenate, a blood-entry component of SFYX, exhibited a strong binding affinity for SIRT3. This study demonstrates that SFYX exerts cardioprotective effects against HF through the deacetylation-regulated activation of SIRT3/FOXO1 signaling-mediated mitophagy and apoptosis. These findings indicate that SFYX represents a promising therapeutic candidate for the treatment of HF.