Chengdu University of Traditional Chinese Medicine (CDUTCM; Chinese: 成都中医药大学; pinyin: Chéngdū zhōng yīyào Dàxué) is located in Chengdu, the capital city of Sichuan province, China. It is also known as Chengdu TCM school. It is a member of Chinese state Double First Class University Plan, with Double First Class University identity identified by the Chinese Ministry of Education.
A new iridoid glycoside (1), along with two known congeners (2−3), was isolated from Lamiophlomis rotata. The structure of new findings was elucidated by comprehensive analyses, including 1D/2D NMR, HRESIMS, hydrolysis derivatization and ECD spectroscopy. Compound 1 shows an obviously anti-inflammatory potential by inhibiting the secretion of NO, iNOS, COX-2 and ROS in LPS-stimulated RAW 264.7 macrophages at the concentration of 7.5 μM.
The global demographic shift toward aging has precipitated a surge in age-related ocular pathologies, imposing a formidable public health challenge that demands urgent intervention. Blinding disorders such as age-related macular degeneration (AMD), cataracts, and dry eye disease exemplify this crisis, with their pathogenesis being intrinsically linked to tissue-specific aging processes in the eye. At the molecular level, core pathways including telomere attrition, oxidative stress, cellular senescence, and autophagic dysregulation orchestrate this degenerative cascade. This review systematically delineates the dynamic interplay network of these pathways during ocular aging, with particular emphasis on four pivotal mechanisms: oxidative stress-driven reactive oxygen species (ROS) accumulation, senescence-associated secretory phenotype (SASP)-mediated inflammatory cascades, autophagic flux dysfunction, and epigenetic remodeling aberrations. We further evaluate recent advancements in translational therapies, emphasizing the clinical potential of targeted gene-editing technologies, stem cell-derived regenerative approaches, and novel senolytic agents. Additionally, artificial intelligence (AI) -assisted diagnostics are explored as pivotal tools for precision medicine, particularly in early disease detection via retinal imaging and biomarker analysis. Future research priorities should focus on the integration of aging-specific biomarkers including methylation signatures, the advancement of tissue-selective drug delivery systems tailored to anterior and posterior ocular compartments. Collectively, these initiatives will propel the development of targeted interventions to address age-related visual decline, positioning precision medicine as the cornerstone of next-generation geriatric ophthalmic care.
Immunotherapy serves as the fourth modality for cancer treatment, following surgery, radiotherapy, and chemotherapy. However, its efficacy remains inconsistent due to the heterogeneity of the tumor microenvironment (TME). Tumors characterized by an immunosuppressive TME that are unresponsive to immunotherapy are termed “cold tumors.” Thus, strategies to reverse this immunosuppressive environment are promising for treating cold tumors. Tumor-associated macrophages (TAMs) play a significant role in this process, making TAM-targeting therapies potentially valuable. Natural products (NPs), which are bioactive compounds from traditional herbs, exhibit broad anticancer effects and modulate TAM polarization, positioning them as a promising source for anticancer agents. This article explores the relationship between TAMs and the TME, emphasizing the mechanisms by which natural products, such as terpenoids and quinones, influence TAM polarization to inhibit tumor progression. By analyzing TAM roles in the TME and summarizing existing natural products targeting TAM polarization, this study offers insights for developing novel TAM-targeting drugs, and aids in the conversion of cold tumors to hot tumors.
Thyroid cancer (TC), the most common endocrine malignancy, presents significant clinical challenges due to the risk of recurrence, metastasis, and treatment resistance, particularly in advanced cases. Driven by lipid peroxidation, ferroptosis is an iron-dependent, regulated cell death pathway increasingly implicated in cancer biology. This review comprehensively summarizes the mechanistic basis of ferroptosis, encompassing iron metabolism, amino acid regulation, lipid peroxidation, and key regulators such as p53, Nrf2, heat shock proteins and its specific implications in thyroid cancer. This study delineates the contribution of both coding and non-coding ferroptosis-related genes as critical modulators of thyroid cancer progression, thereby influencing patient prognosis. The interplay between ferroptosis and the tumor immune microenvironment is also discussed, emphasizing how immune cells like CD8( +)T cells and macrophages influence and respond to ferroptotic signals. Furthermore, we explore the therapeutic potential of targeting ferroptosis using both natural compounds and synthetic agents, which have shown promise in inducing ferroptosis and suppressing tumor growth in preclinical models. Notably, emerging evidence suggests that activating ferroptosis may help overcome radioiodine resistance and improve survival outcomes, particularly in aggressive subtypes such as anaplastic thyroid cancer (ATC). Therefore, the exploitation of ferroptosis offers a promising avenue to address therapeutic resistance and improve prognosis in thyroid cancer, which merits further clinical investigation.
