Olfactory receptors (ORs) form the largest superfamily of G protein-coupled receptors (GPCRs). Traditionally recognized for their role in the nasal olfactory epithelium, where they mediate the sense of smell, accumulating evidence has firmly established their ectopic expression in non-olfactory tissues, including the intestine, lungs, and kidneys. The intestine, as the primary site for nutrient digestion and absorption, harbors a highly complex chemical environment. To adapt to this environment, the gut employs a sophisticated network of “chemosensors” to monitor luminal contents and maintain homeostasis. Among these sensors, intestinal ORs have emerged as crucial functional components, serving as a molecular bridge that connects environmental chemical signals—such as food-derived odorants—to specific physiological responses. This discovery has significantly deepened our understanding of how dietary flavors and compounds influence intestinal physiology at the molecular level. This review systematically summarizes the expression profiles, ligand classification, and biological functions of ORs within the gastrointestinal tract. Studies indicate that intestinal ORs exhibit distinct spatial distribution patterns across different gut segments and display cell-type specificity, particularly within enterocytes and enteroendocrine cells. These receptors function as versatile sensors capable of recognizing a wide variety of ligands, including exogenous dietary components, gut microbiota metabolites such as short-chain fatty acids, and endogenous small molecules like azelaic acid. Upon activation by specific ligands, intestinal ORs trigger intracellular signaling cascades, primarily involving the AC-cAMP-PKA pathway or calcium influx channels. A major focus of this review is to elucidate the molecular mechanisms by which these receptors regulate the secretion of gut hormones. Activation of specific ORs in enteroendocrine cells has been shown to stimulate the release of hormones such as glucagon-like peptide-1 (GLP-1), peptide YY (PYY), and serotonin (5-HT), thereby modulating systemic energy metabolism, glucose homeostasis, and gastrointestinal motility. Furthermore, the review addresses the critical roles of ORs in immune regulation and pathology. Evidence suggests that specific ORs contribute to the maintenance of intestinal immune homeostasis and may offer protection against inflammation. Beyond their involvement in inflammatory responses, ORs such as Olfr78 have been shown to regulate the differentiation and function of intestinal endocrine cells. Similarly, Olfr544 has been demonstrated to alleviate intestinal inflammation by remodeling the gut microbiome and metabolome. These findings collectively suggest that specific ORs hold promise as therapeutic targets for mitigating intestinal inflammation and maintaining gut homeostasis. Additionally, the review explores the emerging role of ORs in cancer. Although OR expression is often downregulated in tumor tissues compared to normal mucosa, activation of specific ORs by certain ligands can inhibit tumor cell proliferation and migration and induce apoptosis via pathways such as MEK/ERK and p38 MAPK. Conversely, other receptors, such as OR7C1, may serve as biomarkers for cancer-initiating cells. In conclusion, intestinal ORs represent a vital component of the gut’s sensory network. The review also discusses the translational potential of these findings. By elucidating the precise pairing relationships between dietary components and specific ORs, novel therapeutic strategies could be developed. Intestinal ORs may thus emerge as promising targets for nutritional and pharmacological interventions in metabolic diseases, inflammatory bowel diseases, and malignancies.

With the continuous deepening of the concept of precision diagnosis and treatment for lung cancer, how to achieve higher efficiency and accuracy in the screening, diagnosis, and treatment pathways in clinical practice has become an important issue that urgently needs to be overcome. The current clinical difficulty lies in the fact that despite continuous advancements in imaging and molecular diagnostic technologies, there are still limitations in manual efficiency and subjective experience when it comes to massive data analysis and multi-scale feature extraction. Artificial intelligence (AI), especially algorithm systems based on deep learning, is an innovative technology capable of deeply empowering medical big data. This method utilizes algorithms such as convolutional neural networks, combined with radiomics, pathomics, and multi-modal data fusion analysis, demonstrating immense potential in early precise detection and benign-malignant differentiation of pulmonary nodules, digital pathological subtype recognition and non-invasive prediction of driver genes, precise 3D surgical planning and automatic delineation of radiotherapy target volumes, as well as dynamic risk warning during follow-up. This innovative technology provides a brand-new solution for realizing intelligent and individualized lung cancer diagnosis and treatment models. This consensus, based on the latest evidence from evidence-based medicine and combined with the development trends in the AI field and real-world clinical needs, was ultimately formed by gathering the consensus opinions of multidisciplinary experts in radiology, pathology, thoracic surgery, and other fields. The main content covers the application specifications of AI in the three core scenarios of lung cancer screening, diagnosis, and treatment, the technical standards for data collection and algorithm validation, as well as the ethical and regulatory challenges faced at the current stage. It aims to clarify the applicable boundaries of AI as a clinical auxiliary decision support tool, providing scientific guidance and standardized exploration directions for peers currently engaged in or planning to carry out AI-assisted clinical diagnosis, treatment, and translation of lung cancer.

OBJECTIVE To investigate the protective effect of Yishen tongluo formula on high glucose-induced injury in renal tubular epithelial cells and its impact on the silence information regulator 3 （SIRT3）-adenosine monophosphate-activated protein kinase （AMPK）/peroxisome proliferator-activated receptor γ coactivator-1α （PGC-1α）/carnitine palmitoyltransferase 1A （CPT1A） signaling pathway. METHODS Human renal tubular epithelial cells HK-2 were used as the subject. The cells were divided into a normal glucose group （NC group）， a high glucose group （HG group）， a high glucose+low-dose Yishen tongluo formula group [HG+L group， 0.5 mg/mL （calculated by crude drugs）]， and a high glucose+high-dose Yishen tongluo formula group [HG+H group， 1.0 mg/mL （calculated by crude drugs）]. Except for the NC group， cells in all other groups were cultured under high glucose conditions （30 mmol/L）， and cells in the HG+L and HG+H groups were simultaneously treated with the corresponding mass concentrations of medicinal liquid. Cell viability was assessed at 0， 24， and 48 h post-incubation， and reactive oxygen species （ROS） level， adenosine triphosphate （ATP） content， and the expression of molecules related to the SIRT3-AMPK/PGC-1α/CPT1A signaling pathway were measured after 48 h of incubation. RESULTS Compared with the NC group， the HG group showed significantly reduced cell viabilities （at 24 and 48 h） and ATP content， along with significantly elevated ROS levels （ P ＜0.05）. Additionally， the protein expressions of SIRT3， PGC-1α and CPT1A， as well as the mRNA expressions of PGC-1α and CPT1A， and the phosphorylation level of AMPK protein were all significantly downregulated or decreased（ P ＜0.05）. Compared with the HG group， the aforementioned indicators were significantly improved in both HG+L and HG+H groups， with the improvement being more pronounced in the HG+H group （ P ＜0.05）. CONCLUSIONS The Yishen tongluo formula can improve high-glucose-induced damage to renal tubular epithelial cells； its action may be related to activating the SIRT3-AMPK/PGC-1α/CPT1A signaling pathway， improving mitochondrial energy metabolism， and alleviating oxidative stress.

OBJECTIVE To investigate the protective effect of Yishen tongluo formula on high glucose-induced injury in renal tubular epithelial cells and its impact on the silence information regulator 3 （SIRT3）-adenosine monophosphate-activated protein kinase （AMPK）/peroxisome proliferator-activated receptor γ coactivator-1α （PGC-1α）/carnitine palmitoyltransferase 1A （CPT1A） signaling pathway. METHODS Human renal tubular epithelial cells HK-2 were used as the subject. The cells were divided into a normal glucose group （NC group）， a high glucose group （HG group）， a high glucose+low-dose Yishen tongluo formula group [HG+L group， 0.5 mg/mL （calculated by crude drugs）]， and a high glucose+high-dose Yishen tongluo formula group [HG+H group， 1.0 mg/mL （calculated by crude drugs）]. Except for the NC group， cells in all other groups were cultured under high glucose conditions （30 mmol/L）， and cells in the HG+L and HG+H groups were simultaneously treated with the corresponding mass concentrations of medicinal liquid. Cell viability was assessed at 0， 24， and 48 h post-incubation， and reactive oxygen species （ROS） level， adenosine triphosphate （ATP） content， and the expression of molecules related to the SIRT3-AMPK/PGC-1α/CPT1A signaling pathway were measured after 48 h of incubation. RESULTS Compared with the NC group， the HG group showed significantly reduced cell viabilities （at 24 and 48 h） and ATP content， along with significantly elevated ROS levels （ P ＜0.05）. Additionally， the protein expressions of SIRT3， PGC-1α and CPT1A， as well as the mRNA expressions of PGC-1α and CPT1A， and the phosphorylation level of AMPK protein were all significantly downregulated or decreased（ P ＜0.05）. Compared with the HG group， the aforementioned indicators were significantly improved in both HG+L and HG+H groups， with the improvement being more pronounced in the HG+H group （ P ＜0.05）. CONCLUSIONS The Yishen tongluo formula can improve high-glucose-induced damage to renal tubular epithelial cells； its action may be related to activating the SIRT3-AMPK/PGC-1α/CPT1A signaling pathway， improving mitochondrial energy metabolism， and alleviating oxidative stress.

Aim To investigate the effect of curcumol(Cur)on apoptosis in senescent Hep3B cells induced by XL413.Methods XL413 induced a senescence model in Hep3B cells.Cur intervention was adminis-tered.CCK-8 and Incucyte? assays were used to eval-uate cell proliferation.Senescence-associated beta-gal-actosidase(SA-β-gal)staining was performed to assess cellular senescence.Flow cytometry was employed to detect apoptosis.RT-qPCR was conducted to measure the mRNA expression levels of senescence-associated secretory phenotype(SASP)factors IL-6,IL-8,and CXCL10.Western blot was performed to assess the ex-pression levels of p16,PI3K,p-PI3K,Akt,p-AKT,Bax,and Bcl-2.The ratios of p-PI3K/PI3K,p-Akt/Akt,and Bcl-2/Bax were calculated.Results Fol-lowing XL413 intervention,the proportion of SA-β-gal-positive cells and the expression of p16 protein signifi-cantly increased compared to the control group(P＜0.05),suggesting the successful establishment of the cell senescence model.CCK-8 assay showed that the IC50 values of Cur intervention in Hep3B cells at 24 h,48 h,and 72 h were 106.40 μmol·L-1,54.67 μmol·L-1,and 31.87 μmol·L-1,respectively.Incucy-te? cell proliferation assay demonstrated that the cell proliferation rate was significantly lower in the XL413 group compared to that in the control group(P＜0.05),and further decreased after Cur intervention(P＜0.05)in a concentration-dependent manner.The proportion of apoptotic cells in the Cur group was sig-nificantly higher than that in the XL413 group(P＜0.05),also exhibiting concentration dependence.Cur intervention led to a significant reduction in IL-6,IL-8,CXCL10 mRNA expression levels,as well as p-PI3K/PI3K and p-AKT/AKT ratios compared to the XL413 group(P＜0.05),with a concentration-de-pendent effect.The expression of Bax protein increased(P＜0.05),while Bcl-2 protein expression decreased and the Bcl-2/Bax ratio decreased(P＜0.05)in the Cur group,showing a dose-dependent effect.Conclu-sions Cur has been shown to clear XL413-induced senescent Hep3B cells,reduce their SASP expression and promote apoptosis.The underlying mechanism may be related to the inhibition of the PI3K/AKT signaling pathway.

China has become the country with the highest global burden of heart failure(HF).Despite the widespread use of prognostic-improving medications today,the mortality rate of HF remains high,reaching 13.7％at one year-particularly among patients with heart failure with reduced ejection fraction(HFrEF).HF interventional device therapy(structural intervention)targets the structural factors underlying HF,including atrial pressure,ventricular remodeling,and valvular intervention.It leverages the heart's intrinsic physiological properties and pathological progression mechanisms to deliver treatments through interventions without external active forces,achieving anatomical or functional repair.This field has emerged as a rapidly growing area and plays an increasingly critical role in HF management.This article provides a comprehensive review and summary of the latest advancements in HF and cardiomyopathy interventional therapy over the past year.It covers various novel technologies and products currently in the research phase,aiming to provide an in-depth analysis of the current status and future directions of HF interventional therapy,and further advance the development of this discipline.

BACKGROUND: Recent studies have shown that sodium-glucose cotransporters-2 (SGLT2) inhibitors significantly improve major adverse cardiovascular events in heart failure with preserved ejection fraction (HFpEF) patients, but the exact mechanism is unknown. Ferritinophagy is a special form of selective autophagy that participates in ferroptosis. In this study, we aimed to investigate whether ferritinophagy was activated during the occurrence of HFpEF, and whether canagliflozin (CANA) could inhibite ferritinophagy. METHODS: We reared Dahl salt-sensitive (DSS) rats on a high-salt diet to construct a hypertensive HFpEF model, and simultaneously administered CANA intervention. Then we detected indicators related to ferritinophagy. RESULTS: The expression of nuclear receptor coactivator 4 (NCOA4), as well as microtubule-associated proteins light chain 3 (LC3), Bcl-2 interacting protein 1 (Beclin-1) and p62, were upregulated in HFpEF rats, accompanied by the downregulation of ferritin heavy chain 1 (FTH1), upregulation of mitochondrial iron transporter sideroflexin1 (SFXN1) and increased reactive oxygen species (ROS) production. Above changes were diminished by CANA. CONCLUSION Ferritinophagy is activated in HFpEF rats and then inhibited by CANA, leading to HFpEF benefits. The inhibition of ferritinophagy could provide new prospective targets for the prevention and treatment of HFpEF, and provide new ideas for investigating the mechanism of cardiovascular benefit of SGLT2 inhibitors.

Olfactory disorders are a common symptom in patients with chronic rhinosinusitis, and their diagnosis and treatment have garnered extensive attention from both patients and doctors. Currently, there are various evaluation and treatment methods for olfactory dysfunction; however, choosing a simpler and more accurate assessment, as well as an effective treatment, remains a clinical challenge. In this article, we review the assessment and treatment methods commonly used in clinical practice in recent years to provide better support for the diagnosis and treatment of olfactory disorders.
Humans ; Olfaction Disorders/etiology* ; Sinusitis/complications* ; Chronic Disease ; Rhinitis/complications* ; Rhinosinusitis