Osteoporosis (OP) is a systemic skeletal disorder characterized by decreased bone mineral density (BMD), impaired bone microarchitecture, and an elevated risk of fragility fractures. Although conventional pharmacological agents—such as bisphosphonates, selective estrogen receptor modulators, and monoclonal antibodies—can attenuate disease progression, their long-term application is limited by adverse effects and suboptimal patient adherence. Consequently, there is growing interest in the development of safer, multi-targeted therapeutic strategies. Plant-derived bioactive products have garnered increasing attention due to their broad pharmacological profiles, including the promotion of osteoblastogenesis, suppression of osteoclastogenesis, regulation of bone–vascular coupling, and modulation of immune and oxidative stress pathways. Recent advances in biomaterial-assisted delivery systems have further improved the physicochemical stability, bioavailability, and tissue-specific delivery of these phytochemicals, thereby enhancing their therapeutic efficacy in bone regeneration. Although accumulated in vitro and in vivo studies suggest the bone-protective potential of these natural agents, clinical translation remains limited. Further mechanistic investigations and rigorously designed clinical trials are warranted to substantiate their efficacy and safety in human populations. This review summarizes recent progress in the mechanistic understanding of natural products involved in bone metabolism, with a particular focus on representative classes such as flavonoids, polyphenols, polysaccharides, glycosides, and terpenoids. In addition, we discuss the translational potential of integrating these agents with advanced drug delivery platforms, aiming to provide a theoretical framework and future research directions for the treatment of OP and related bone disorders.

Ziziphi Spinosae semen (ZSS) is renowned for its rich nutritional composition and is traditionally consumed in China, Japan, and Korea, where it is widely incorporated into both medicinal diets and daily cuisine. To address the lack of systematic research comparing raw and fried ZSS, this study aimed to elucidate the compositional and functional changes induced by the frying process. This study systematically compared the chemical profiles and antioxidant activities of ZSS and fried ZSS using ultra-performance liquid chromatography–quadrupole–time-of-flight mass spectrometry (UPLC–Q–TOF–MS) and gas chromatography–ion mobility spectrometry (GC–IMS). A total of 92 non-volatile compounds and 43 volatile organic compounds (VOCs) were identified. Frying significantly promoted the formation of polar compounds such as flavonoids and saponins and increased the content of aldehydes and alcohols, thereby generating aromas characteristic of Maillard reactions and lipid oxidation. Principal component analysis (PCA) and orthogonal partial least squares discriminant analysis (OPLS-DA) clearly distinguished the two groups in terms of their chemical composition and flavor characteristics. In addition, 2,2-diphenyl-1-picrylhydrazyl (DPPH) and 2,2′-azino-bis (3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) assays demonstrated that the antioxidant capacity of fried ZSS was significantly higher than that of the raw sample (p < 0.05). These results indicate that the frying process reshapes the chemical properties and bioactivity of ZSS via multiple pathways, including glycoside hydrolysis, lipid oxidation, and Maillard reactions. Overall, this study establishes a scientific foundation for the development of functional foods derived from ZSS.

Ovarian aging, marked by follicle depletion and oocyte quality decline, involves complex metabolic alterations. This review synthesizes evidence that dysregulated metabolic reprogramming, encompassing energy, lipid, and nutrient metabolism, drives ovarian functional decline. Central to this process is a self-reinforcing “metabolism-epigenetics-immunity” triangular network, where mitochondrial dysfunction and NAD⁺ depletion disrupt epigenetic regulation and activate chronic inflammation, collectively accelerating follicular atresia and hormonal dysfunction. By integrating this mechanistic framework, we highlight emerging intervention strategies targeting metabolic hubs, such as mitochondrial rescue and senescent cell clearance, which offer new avenues for preserving ovarian function. This work provides a conceptual foundation for developing personalized strategies to mitigate reproductive aging and its systemic health impacts.

Ovarian diseases including polycystic ovary syndrome (PCOS), premature ovarian insufficiency (POI) and ovarian cancer, critically impact women’s repr

Osteoporosis is a metabolic bone disease characterized by the loss and destruction of bone microstructure. Its incidence rate increases with age and is an important public health problem. Recently, the relationship between lipid metabolism and osteoporosis has received widespread attention. Lipid metabolites, such as fatty acids, cholesterol, and adipose tissue-derived hormones, participate in maintaining bone metabolism homeostasis through key molecular networks that regulate bone cell function. In addition, the interaction between lipid metabolism and bone tissue involves cross-organ regulatory mechanisms, including the bone-adipose, bone-pancreas, and bone-gut axes. This study considers the types of lipid metabolites and their effects on bone cell function as a starting point for exploring the interaction between lipid metabolism and bone tissue. Furthermore, this study elucidated the specific mechanism of action of lipid metabolites on osteocytes, analyzed the relationship between lipid metabolism abnormalities and osteoporosis, and provided ideas for further clinical research on lipid metabolism-related osteoporosis.

Heart failure (HF) represents the terminal stage of multiple cardiovascular disorders and is characterized by substantial morbidity, disability, and mortality. Although standard pharmacotherapies offer partial symptomatic relief, their capacity to halt or reverse disease progression remains limited. In recent years, autophagy—an essential intracellular degradation and recycling process that safeguards cardiomyocyte homeostasis—has emerged as a critical determinant in the onset and progression of HF. In this review, we systematically examined approximately 170 research articles related to “natural compounds-autophagy-HF” published up to 2025, and synthesized major advances reported over the past five years. Based on chemical structure and natural source, representative bioactive compounds were categorized into five major classes: flavonoids, polyphenols, alkaloids, terpenoids, and marine-derived molecules. We then integrated evidence on the principal autophagy-regulatory signaling cascades influenced by these compounds, including the AMP-activated protein kinase (AMPK)/mechanistic target of rapamycin (mTOR) axis, phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt), sirtuin 1 (SIRT1)/forkhead box O (FOXO), BCL2/adenovirus E1B 19 kDa-interacting protein 3 (BNIP3)/NIP3-like protein X (NIX), and Beclin-1 pathways. Moreover, this review summarizes how these natural compounds modulate autophagy to attenuate key pathological processes associated with HF, including cardiac hypertrophy, adverse ventricular remodeling, mitochondrial dysfunction, and cardiomyocyte apoptosis. By comparing convergent mechanisms and compound-specific differences in autophagy-mediated cardioprotection, we highlight emerging mechanistic patterns and therapeutic implications. Collectively, through structured classification of compounds, integration of autophagy signaling pathways, and assessment of translational potential, this review provides a systematic framework to guide the rational application and further development of natural products for the prevention and treatment of HF. Graphical abstract