Acta Biochimica et Biophysica Sinica•2026•DOI: 10.3724/abbs.2025195
Chronic psychosocial stress is increasingly recognized as a key risk factor for dry eye disease, potentially because of its disruption of the circadian transcriptome and lacrimal gland function, which impacts eye health. In this study, we test this hypothesis by using two mouse models (high platform and restraint experiments) of psychological stress and report that both models uniquely alter the circadian transcriptome and signaling pathways of the lacrimal gland. Psychosocial stress significantly affects the normal rhythmic oscillations of extraorbital lacrimal gland (ELG) immune cell trafficking, secretion response, and lipid deposition. Both models significantly reduce the volume of stimulated lacrimal secretions as well as the recruitment of immune cells to the lacrimal gland. Importantly, treatment with beta-adrenergic receptor blockers or glucocorticoid synthesis inhibitors significantly improves these secretory functions and histopathological changes. Collectively, these findings demonstrate the detrimental effects of chronic psychosocial stress on lacrimal gland circadian transcriptome homeostasis and suggest potential clinical applications for patients with both psychological stress and dry eye disease.
Acta Biochimica et Biophysica Sinica•2026•DOI: 10.3724/abbs.2025221
Hypertension is commonly accompanied by endothelial dysfunction, characterized by an imbalance between vasodilatation and constriction, increased levels of the proinflammatory factors interleukin-6 (IL-6) and intercellular adhesion molecule-1 (ICAM-1), and decreased nitric oxide (NO) bioavailability. Using an angiotensin II (Ang II)-induced endothelial dysfunction model, we show that treatment with the hydrogen sulfide (H₂S) donor GYY4137 significantly reverses Ang II-induced damage. GYY4137 restores sirtuin 6 (SIRT6) expression, suppresses inflammation, and improves vasodilatory function. Furthermore, endothelial-specific cystathionine-γ-lyase (CSE)-deficient mice exhibit inflammation and endothelial dysfunction in blood vessels, which is reversed by H₂S supplementation. Critically, SIRT6 inhibitors block the protective effects of H₂S in the endothelium. This study demonstrates that H₂S protects vascular endothelial function by activating the SIRT6 anti-inflammatory pathway.
Chinese Journal of Tissue Engineering Research•2026•DOI: 10.12307/2026.21612
BACKGROUND: Understanding the characteristics of lung tissue repair and risk factors in patients with chronic obstructive pulmonary disease (COPD) is crucial for improving disease management and enhancing patient quality of life. Existing clinical indicators cannot accurately quantify the tissue repair potential and disease progression risk in patients with a history of frequent hospitalizations. OBJECTIVE: To conduct a risk prediction model analysis of lung tissue repair mechanisms in COPD based on computer simulation and case validation, thereby promoting lung tissue repair/regeneration in COPD patients, reducing the frequency of hospitalizations, and improving quality of life. METHODS: Medical records from 200 patients with COPD hospitalized at Beijing Jingmei Group General Hospital from 2022-10-01 to 2023-10-01 were collected. Patients were grouped based on the number of hospitalizations for COPD within 1 year after discharge: 100 patients with ≥2 hospitalizations were assigned to the frequent hospitalization group, and 100 patients with <2 hospitalizations were assigned to the non-frequent hospitalization group. General clinical data, pulmonary function, blood gas analysis, and hematological indicators were compared between the two groups. Variables with P < 0.05 were included in a multivariate logistic regression model to identify risk factors for rehospitalization within 1 year. The area under the receiver operating characteristic curve (AUC) was used to evaluate the predictive efficacy of the clinical risk factor model. RESULTS AND CONCLUSION: (1) Pulmonary function: There were significant differences between the two groups in FEV1% predicted, FVC, FVC% predicted, FEV1/FVC, residual volume/total lung capacity ratio, diffusing capacity of the lung for carbon monoxide (DLCO), and DLCO/alveolar volume (P < 0.05). (2) Blood gas analysis: Significant differences were found in oxygen partial pressure, carbon dioxide partial pressure, oxygen saturation, and respiratory failure type (P < 0.05). (3) Hematological indicators: Significant differences were observed in absolute neutrophil count, D-dimer, absolute lymphocyte count, neutrophil percentage, and red blood cell distribution width (RDW) (P < 0.05), while no significant differences were found in eosinophil percentage, fibrinogen, and absolute eosinophil count (P > 0.05). (4) Logistic regression analysis showed that FEV1% predicted (OR=1.01, 95%CI: 1.004-1.017, P=0.011), DLCO (OR=2.28, 95%CI: 1.270-3.025, P=0.004), type I respiratory failure (OR=3.15, 95%CI: 2.414-5.947, P=0.001), type II respiratory failure (OR=7.03, 95%CI: 1.688-8.604, P=0.001), and RDW (OR=1.50, 95%CI: 0.65-3.44, P < 0.0001) were risk factors for frequent hospitalizations in COPD patients. (5) ROC curve analysis showed that when FEV1% predicted was below 52.9%, DLCO below 4 mmol/(min·kPa), presence of type I respiratory failure, or RDW above 14.5%, the risk of frequent hospitalizations increased. (6) The logistic regression model and ROC curve analysis indicated that severely impaired diffusion capacity, combined respiratory failure, and elevated RDW are major risk factors for frequent hospitalizations in COPD patients. Early identification and intervention of these factors are important for improving lung tissue repair potential, predicting disease progression risk, and enhancing quality of life.
Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2025221
Hypertension is commonly accompanied by endothelial dysfunction, characterized by an imbalance between vasodilatation and constriction, increased levels of the proinflammatory factors interleukin-6 (IL-6) and intercellular adhesion molecule-1 (ICAM-1), and decreased nitric oxide (NO) bioavailability. Using an angiotensin II (Ang II)-induced endothelial dysfunction model, we show that treatment with the hydrogen sulfide (H₂S) donor GYY4137 significantly reverses Ang II-induced damage. GYY4137 restores sirtuin 6 (SIRT6) expression, suppresses inflammation, and improves vasodilatory function. Furthermore, endothelial-specific cystathionine-γ-lyase (CSE)-deficient mice exhibit inflammation and endothelial dysfunction in blood vessels, which is reversed by H₂S supplementation. Critically, SIRT6 inhibitors block the protective effects of H₂S in the endothelium. This study demonstrates that H₂S protects vascular endothelial function by activating the SIRT6 anti-inflammatory pathway.