Plant- and marine-derived natural products are rich sources of bioactive compounds essential for drug discovery. These compounds contain complex mixtures of metabolites, which collectively contribute to their pharmacological properties. However, challenges arise in the isolation of individual bioactive compounds, owing to their intricate chemistry and low abundance in natural extracts. Despite these limitations, numerous plant and marine-derived compounds have achieved regulatory approval, particularly for treating cancer and infectious diseases. This review explores the therapeutic potential of plant and marine sources along with innovative extraction and isolation methods that support sustainable drug development. Future perspectives will highlight the role of responsible innovation, artificial intelligence, and machine learning in advancing drug discovery, underscoring the importance of continued research to meet global health needs.

Bone marrow mesenchymal stem cell-derived exosomal microRNAs target PI3K/Akt signaling pathway to promote the activation of fibroblasts

Vasorin (VASN) is an important transmembrane protein associated with development and disease. However, it is not clear whether the death of mice with VASN deficiency (VASN^−/−) is related to cardiac dysfunction. The aim of this research was to ascertain whether VASN induces pathological cardiac hypertrophy by targeting myosin light chain 7 (MYL7). VASN^−/− mice were produced by CRISPR/Cas9 technology and inbreeding. PCR amplification, electrophoresis, real‐time PCR and Western blotting were used to confirm VASN deficiency. Cardiac hypertrophy was examined by blood tests, histological analysis and real‐time PCR, and key downstream factors were identified by RNA sequencing and real‐time PCR. Western blotting, immunohistochemistry and electron microscopy analysis were used to confirm the downregulation of MYL7 production and cardiac structural changes. Our results showed that sudden death of VASN^−/− mice occurred 21–28 days after birth. The obvious increases in cardiovascular risk, heart weight and myocardial volume and the upregulation of hypertrophy marker gene expression indicated that cardiac hypertrophy may be the cause of death in young VASN^−/− mice. Transcriptome analysis revealed that VASN deficiency led to MYL7 downregulation, which induced myocardial structure abnormalities and disorders. Our results revealed a pathological phenomenon in which VASN deficiency may lead to cardiac hypertrophy by downregulating MYL7 production. However, more research is necessary to elucidate the underlying mechanism.

Rotator cuff tendon-bone healing is impeded by inflammation and inadequate regeneration. This study evaluates exosome-mimetics (EMs) derived from stem cells of human exfoliated deciduous teeth (SHEDs) as a therapeutic strategy to enhance repair.SHED-EMs were synthesized via serial extrusion and characterized using transmission electron microscopy, nanoparticle tracking analysis, and Western blot. In vitro experiments assessed biocompatibility, tenogenic differentiation of tendon stem/progenitor cells (TSPCs), chondrogenic differentiation of bone marrow stromal cells (BMSCs), and macrophage polarization (Raw264.7 cells). Transcriptomic sequencing of LPS-stimulated macrophages and autophagy inhibition (via 3-MA) were conducted to explore mechanisms. A rat rotator cuff tear model treated with GM@PDA&EMs hydrogel was analyzed through histology, micro-CT, and biomechanical testing.SHED-EMs exhibited uniform morphology (average 124.9 nm) and high yield (57.6 μg per T25 flask). They promoted TSPC tenogenesis (increased COL I, Tnmd, Scx) and BMSC chondrogenesis (elevated Col II, Acan, Sox9). SHED-EMs polarized macrophages toward the M2 phenotype (reduced CD86/iNOS, increased CD163), reversing M1-mediated suppression of BMSC osteogenesis (enhanced Runx2, OCN) and HUVEC angiogenesis (upregulated VEGF, CD31). In vivo, GM@PDA&EMs reduced M1 macrophage infiltration, enhanced osteocalcin and VEGF expression, and improved biomechanical strength. Transcriptomic analysis of macrophages revealed SHED-EMs suppressed NF-κB signaling, while subsequent experiments demonstrated autophagy activation (increased LC3II/I, decreased P62) and reduced inflammation (lower TNF-α/iNOS). Autophagy inhibition abolished these anti-inflammatory effects. SHED-EMs accelerates tendon-bone healing by modulating macrophage polarization, enhancing tissue regeneration, and suppressing NF-κB-mediated inflammation via autophagy activation, offering a promising therapy for rotator cuff injuries.

Hypertension and dyslipidemia were important risk factors for cardiovascular diseases. This study adhered to stringent inclusion and exclusion criteria, ultimately incorporating 3522 participants for analysis. Data analysis included univariate regression, LASSO regression, and multifactorial regression to screen for key risk factors. The predictive power of the model was assessed by a nomogram model and ROC curve. Among matched patients with hypertension and dyslipidemia, the proportion of females was significantly higher than that of males ( P < 0.001), and BMI increased significantly ( P < 0.001). Univariate analysis showed that PLT, BMI, RSBP, TBIL, FBG, BUN, and smoking status were significantly associated with dyslipidemia ( P < 0.05). PLT, BMI, and FBG contributed the most to the prediction of dyslipidemia. The ROC curve AUC of the nomogram model was 0.639, showing moderate predictive power, and the significance of these indicators was further verified by the Delong test ( P < 0.001). ROC analysis showed high sensitivity and specificity for PLT, BMI, and FBG. This study found that the prevalence of dyslipidemia in hypertensive patients was significant and correlated with multiple factors, and BMI, PLT, and FBG were the most important predictors. The nomogram model was able to predict the occurrence of dyslipidemia at a moderate level.