Unique regulatory network of dragon fruit simultaneously mitigates the effect of vanadium pollutant and environmental factors.

Under changing climatic conditions, plants are simultaneously facing conflicting stresses in nature. Plants can sense different stresses, induce systematic ROS signals, and regulate transcriptomic, hormonal, and stomatal responses. We performed transcriptome analysis to reveal the integrative stress response regulatory mechanism underlying heavy metal stress alone or in combination with heat and drought conditions in pitaya (dragon fruit). A total of 70 genes were identified from 31,130 transcripts with conserved differential expression. Furthermore, weighted gene co-expression network analysis (WGCNA) identified trait-associated modules. By integrating information from three modules and protein-protein interaction (PPI) networks, we identified 10 interconnected genes associated with the multifaceted defense mechanism employed by pitaya against co-occurring stresses. To further confirm the reliability of the results, we performed a comparative analysis of 350 genes identified by three trait modules and 70 conserved genes exhibiting their dynamic expression under all treatments. Differential expression pattern of genes and comparative analysis, have proven instrumental in identifying ten putative structural genes. These ten genes were annotated as PLAT/LH2, CAT, MLP, HSP, PB1, PLA, NAC, HMA, and CER1 transcription factors involved in antioxidant activity, defense response, MAPK signaling, detoxification of metals and regulating the crosstalk between the complex pathways. Predictive analysis of putative candidate genes, potentially governing single, double, and multifactorial stress response, by several signaling systems and molecular patterns. These findings represent a valuable resource for pitaya breeding programs, offering the potential to develop resilient "super pitaya" plants.

Dietary fiber alleviates alcoholic liver injury via Bacteroides acidifaciens and subsequent ammonia detoxification.

The gut microbiota and diet-induced changes in microbiome composition have been linked to various liver diseases, although the specific microbes and mechanisms remain understudied. Alcohol-related liver disease (ALD) is one such disease with limited therapeutic options due to its complex pathogenesis. We demonstrate that a diet rich in soluble dietary fiber increases the abundance of Bacteroides acidifaciens (B. acidifaciens) and alleviates alcohol-induced liver injury in mice. B. acidifaciens treatment alone ameliorates liver injury through a bile salt hydrolase that generates unconjugated bile acids to activate intestinal farnesoid X receptor (FXR) and its downstream target, fibroblast growth factor-15 (FGF15). FGF15 promotes hepatocyte expression of ornithine aminotransferase (OAT), which facilitates the metabolism of accumulated ornithine in the liver into glutamate, thereby providing sufficient glutamate for ammonia detoxification via the glutamine synthesis pathway. Collectively, these findings uncover a potential therapeutic strategy for ALD involving dietary fiber supplementation and B. acidifaciens.

Imidazole-Based Ionic Liquid Engineering for Perovskite Solar Cells with High Efficiency and Excellent Stability.

Despite the remarkable progress of perovskite solar cells (PSCs), the substantial inherent defects within perovskites restrict the achievement of higher efficiency and better long-term stability. Herein, we introduced a novel multifunctional imidazole analogue, namely, 1-benzyl-3-methylimidazolium bromide (BzMIMBr), into perovskite precursors to reduce bulk defects and inhibit ion migration in inverted PSCs. The electron-rich environment of -N- in the BzMIMBr structure, which is attributed to the electron-rich adjacent benzene ring-conjugated structure, effectively passivates the uncoordinated Pb2+ cations. Moreover, the interaction between the BzMIMBr additive and perovskite can effectively hinder the deprotonation of formamidinium iodide/methylammonium iodide (FAI/MAI), extending the crystallization time and improving the quality of the perovskite precursors and films. This interaction also effectively inhibits ion migration to subsequent deposited films, leading to a noteworthy decrease in trap states. Various characterization studies show that the BzMIMBr-doped films exhibit superior film morphology and surface uniformity and reduced nonradiative carrier recombination, consequently enhancing crystallinity by reducing bulk/surface defects. The PSCs fabricated on the BzMIMBr-doped perovskite thin film exhibit a power conversion efficiency of 23.37%, surpassing that of the pristine perovskite device (20.71%). Additionally, the added BzMIMBr substantially increased the hydrophobicity of perovskite, as unencapsulated devices still retained 93% of the initial efficiency after 1800 h of exposure to air (45% relative humidity).

Human placental mesenchymal stromal cells promote the formation of CD8+CD122+PD-1+Tregs via CD73/Foxo1 to alleviate liver injury in graft-versus-host disease mice.

BACKGROUND: Human placental mesenchymal stromal cells (hPMSCs) are known to limit graft-versus-host disease (GVHD). CD8+CD122+PD-1+Tregs have been shown to improve the survival of GVHD mice. However, the regulatory roles of hPMSCs in this subgroup remain unclear. Here, the regulatory mechanism of hPMSCs in reducing liver fibrosis in GVHD mice by promoting CD8+CD122+PD-1+Tregs formation and controlling the balance of IL-6 and IL-10 were explored. METHODS: A GVHD mouse model was constructed using C57BL/6J and BALB/c mice and treated with hPMSCs. LX-2 cells were explored to study the effects of IL-6 and IL-10 on the activation of hepatic stellate cells (HSCs). The percentage of CD8+CD122+PD-1+Tregs and IL-10 secretion were determined using FCM. Changes in hepatic tissue were analysed by HE, Masson, multiple immunohistochemical staining and ELISA, and the effects of IL-6 and IL-10 on LX-2 cells were detected using western blotting. RESULTS: hPMSCs enhanced CD8+CD122+PD-1+Treg formation via the CD73/Foxo1 and promoted IL-10, p53, and MMP-8 levels, but inhibited IL-6, HLF, α-SMA, Col1α1, and Fn levels in the liver of GVHD mice through CD73. Positive and negative correlations of IL-6 and IL-10 between HLF were found in liver tissue, respectively. IL-6 upregulated HLF, α-SMA, and Col1α1 expression via JAK2/STAT3 pathway, whereas IL-10 upregulated p53 and inhibited α-SMA and Col1α1 expression in LX-2 cells by activating STAT3. CONCLUSIONS: hPMSCs promoted CD8+CD122+PD-1+Treg formation and IL-10 secretion but inhibited HSCs activation and α-SMA and Col1α1 expression by CD73, thus controlling the balance of IL-6 and IL-10, and alleviating liver injury in GVHD mice.

A novel bispecific peptide targeting PD-1 and PD-L1 with combined antitumor activity of T-cells derived from the patients with TSCC.

Programmed death-1 (PD-1) and programmed death ligand-1 (PD-L1) are key immune checkpoints (ICs) that critically influence immunotherapy. Tumor resistance to single IC-targeting drugs has increased interest in dual-target drugs, which have shown feasibility for cancer treatment. In this study, we aimed to develop dual-target peptide drugs targeting the PD-1/PD-L1 pathway and to evaluate their efficacy compared to functional antibodies in enhancing the cytotoxicity of human T cells against tongue squamous carcinoma cell lines. Through sequence analysis and peptide truncation, we modified a pre-existing peptide named nABPD-1 targeting PD-1. Subsequently, we obtained two novel peptides named nABPD-2 and nABPD-3, with nABPD-2 showing an enhanced affinity for human PD-1 protein compared to nABPD-1. Importantly, nABPD-2 exhibited dual-targeting capability, possessing a high affinity for both PD-L1 and PD-1. Furthermore, nABPD-2 effectively promoted the cytotoxicity of human T cells against tongue squamous carcinoma cell lines, surpassing the efficacy of anti-PD-1 or anti-PD-L1 functional antibodies alone. Considering that nABPD-2 has lower production costs and dose requirements, it can potentially be used in therapeutic applications.

Rab11b promotes M1-like macrophage polarization by restraining autophagic degradation of NLRP3 in alcohol-associated liver disease.

Macrophage polarization is vital to mounting a host defense or repairing tissue in various liver diseases. Excessive activation of the NLR family pyrin domain containing 3 (NLRP3) inflammasome is related to the orchestration of inflammation and alcohol-associated liver disease (ALD) pathology. Rab GTPases play critical roles in regulating vesicular transport. In this study we investigated the role of Rab11b in ALD, aiming to identify effective therapeutic targets. Here, we first demonstrated a decreased expression of Rab11b in macrophages from ALD mice. Knockdown of Rab11b by macrophage-specific adeno-associated virus can alleviate alcohol induced liver inflammation, injury and steatosis. We found that LPS and alcohol stimulation promoted Rab11b transferring from the nucleus to the cytoplasm in bone marrow-derived macrophages (BMDM) cells. Rab11b specifically activated the NLRP3 inflammasome in BMDMs and RAW264.7 cells to induce M1 macrophage polarization. Rab11b overexpression in BMDMs inhibited autophagic flux, leading to the suppression of LC3B-mediated NLRP3 degradation. We conclude that impaired Rab11b could alleviate alcohol-induced liver injury via autophagy-mediated NLRP3 degradation.

Clinical application of the dissection of the preperitoneal space without electrocoagulation in laparoscopic transperitoneal inguinal hernia repair throughout of the whole process.

Introduction: The dissection of the preperitoneal space is performed using a monopolar instrument to prevent bleeding in laparoscopic transabdominal preperitoneal hernia repair (TAPP). It may also cause energy injuries and nerve damage. Aim: To assess the effectiveness and safety of dissection of the preperitoneal space without electrocoagulation (DPSWE) in TAPP throughout the process. Material and methods: A retrospective analysis of data of 134 patients was made. The electrocoagulation group (EG) relied on monopolar instruments. In the non-electrocoagulation group (NEG) mainly scissors were used without electrocoagulation. The patients were followed for up for 3 months. Intraoperative and postoperative conditions and other complications were observed. Results: The VAS scores in the NEG were lower than those in the EG (p < 0.05). The operation time in the NEG was shorter than that in the EG (p < 0.05). Hospitalization expenses, scrotal seroma formation, and rupture of hernia sac in the NEG were lower than those in the EG (p < 0.05). The intraoperative bleeding volume above 20 ml in the NEG was higher than that in the EG. There was no significant difference in the incidence of postoperative bleeding, vas deferens injury, intestinal injury, surgical site infection, length of hospital stay, urinary retention and hernia recurrence in the NEG and the EG (p > 0.05). There was no significant difference in the incidence of surgical site infections (SSIs) in the NEG and the EG. Conclusions: DPSWE is effective and safe. DPSWE may reduce postoperative pain and have no significant increase in postoperative bleeding.

Melatonin Ameliorates Depressive-Like Behaviors in Ovariectomized Mice by Improving Tryptophan Metabolism via Inhibition of Gut Microbe Alistipes Inops.

Melatonin (N-acetyl-5-methoxytryptamine) is reported to improve mood disorders in perimenopausal women and gut microbiome composition is altered during menopausal period. The possible role of microbiome in the treatment effect of melatonin on menopausal depression remains unknown. Here, it is shown that melatonin treatment reverses the gut microbiota dysbiosis and depressive-like behaviors in ovariectomy (OVX) operated mice. This effect of melatonin is prevented by antibiotic cocktails (ABX) treatment. Transferring microbiota harvested from adolescent female mice to OVX-operated mice is sufficient to ameliorate depressive-like behaviors. Conversely, microbiota transplantation from OVX-operated mice or melatonin-treated OVX-operated mice to naïve recipient mice exhibits similar phenotypes to donors. The colonization of Alistipes Inops, which is abundant in OVX-operated mice, confers the recipient with depressive-like behaviors. Further investigation indicates that the expansion of Alistipes Inops induced by OVX leads to the degradation of intestinal tryptophan, which destroys systemic tryptophan availability. Melatonin supplementation restores systemic tryptophan metabolic disorders by suppressing the growth of Alistipes Inops, which ameliorates depressive-like behaviors. These results highlight the previously unrecognized role of Alistipes Inops in the modulation of OVX-induced behavioral disorders and suggest that the application of melatonin to inhibit Alistipes Inops may serve as a potential strategy for preventing menopausal depressive symptoms.

Adolescent co-exposure to environmental cadmium and high-fat diet induces cognitive decline via Larp7 m6A-mediated SIRT6 inhibition.

The effects and underlying mechanisms of adolescent exposure to combined environmental hazards on cognitive function remain unclear. Here, using a combined exposure model, we found significant cognitive decline, hippocampal neuronal damage, and neuronal senescence in mice exposed to cadmium (Cd) and high-fat diet (HFD) during adolescence. Furthermore, we observed a significant downregulation of Sirtuin 6 (SIRT6) expression in the hippocampi of co-exposed mice. UBCS039, a specific SIRT6 activator, markedly reversed the above adverse effects. Further investigation revealed that co-exposure obviously reduced the levels of La ribonucleoprotein 7 (LARP7), disrupted the interaction between LARP7 and SIRT6, ultimately decreasing SIRT6 expression in mouse hippocampal neuronal cells. Overexpression of Larp7 reversed the combined exposure-induced SIRT6 decrease and senescence in mouse hippocampal neuronal cells. Additionally, the results showed notably elevated levels of Larp7 m6A and YTH domain family protein 2 (YTHDF2) in mouse hippocampal neuronal cells treated with the combined hazards. Ythdf2 short interfering RNA, RNA immunoprecipitation, and RNA stability assays further demonstrated that YTHDF2 mediated the degradation of Larp7 mRNA under combined exposure. Collectively, adolescent co-exposure to Cd and HFD causes hippocampal senescence and cognitive decline in mice by inhibiting LARP7-mediated SIRT6 expression in an m6A-dependent manner.

Construction of direct Z-scheme Co9S8/CdS with tubular heterostructure through the simultaneous immobilization and in-situ reduction strategy for enhanced photocatalytic Cr(VI) reduction under visible light.

Tubular Co9S8/CdS heterostructures have been successfully synthesized by in-situ growing CdS onto Co9S8 nanotubes through a simultaneous immobilization and in-situ reduction strategy. It turned out that the so-obtained heterostructure with Co9S8/CdS molar ratio of 1/10 can display a broad light absorption edge and especially much enhanced capacity for photocatalytic reduction of Cr(VI) under visible light. The characterization analysis and experimental results suggested that an interfacial electrostatic field between Co9S8 and CdS elements in the heterostructure could be constructed due to their different Fermi levels, allowing for more quantities of highly reductive electrons to participate in the photocatalytic reaction. Therefore, the so-obtained Co9S8/CdS (1/10) heterostructures could achieve the photocatalytic reduction efficiency of 100% within 20 min, which was more than two and four times larger than that of pristine CdS and Co9S8, respectively. Moreover, the possible photocatalytic reaction mechanism for reducing Cr(VI) was investigated and found to follow the direct Z-scheme charge transfer pathway. This novel fabrication route for composite photocatalysts with tubular heterostructures could lead to the widespread implementations for the elimination of various harmful pollutants in the process of environmental governance.

Causal relationships of lifestyle behaviours and body fat distribution on diabetic microvascular complications: a Mendelian randomization study.

Objectives: To determine the causal correlations of lifestyle behaviours and body fat distribution on diabetic microvascular complications through a Mendelian Randomization (MR). Methods: Genetic variants significantly associated with lifestyle behaviours, abdominal obesity, generalized obesity and diabetic microvascular complications were extracted from the UK Biobank (UKB) and FinnGen. The inverse variance weighted (IVW) method was regarded as the primary method. The main results were presented in odds ratio (OR) per standard deviation (SD) increase, and a series of sensitivity analyses were also conducted to validate the stability of the results. Results: There was a positive causal correlation between smoking and the development of diabetic retinopathy (OR = 1.16; 95%CI: 1.04-1.30; p = 0.01). All of the indicators representing abdominal obesity had a statistically significant causal association with diabetic microvascular complications. Concerning generalized obesity, there were significant causal associations of body mass index (BMI) on diabetic nephropathy (OR = 1.92; 95%CI: 1.58-2.33; p < 0.001), diabetic retinopathy (OR = 1.27; 95%CI: 1.15-1.40; p < 0.001), and diabetic neuropathy (OR = 2.60; 95%CI: 1.95-3.45; p < 0.001). Other indicators including leg fat mass (left), and arm fat mass (left) also had a significant positive causality with diabetic microvascular complications. Conclusion: Our findings suggested that smoking has a genetically causal association with the development of diabetic retinopathy rather than diabetic nephropathy and diabetic neuropathy. In addition, both abdominal obesity and generalized obesity are risk factors for diabetic microvascular complications. To note, abdominal obesity represented by waist circumference (WC) is the most significant risk factor.

Role of frailty in predicting outcomes after stroke: a systematic review and meta-analysis.

Background: Stroke is considered the second most common cause of death and the third leading cause of disability worldwide. Frailty, characterized by increased vulnerability to stressors, is emerging as a key factor affecting outcomes in older adults and stroke patients. This study aimed to estimate the prevalence of frailty in acute stroke patients and assess its association with mortality and poor functional outcome. Methods: Medline, Google Scholar, and Science Direct databases were systematically searched for English-language studies that included adult stroke patients (>16 years), have defined frailty, and reported mortality and functional outcomes. Meta-analysis was done using STATA 14.2, and the results were expressed as pooled odds ratios (OR) with 95% confidence intervals (CI). Heterogeneity was assessed using the I2 statistic and the Chi-square test. Study quality was evaluated using the Newcastle Ottawa Scale (NOS). Results: Twenty-five studies were included in the analysis. Frailty prevalence in stroke patients was 23% (95% CI 22% - 23%). Unadjusted analysis showed an OR of 2.66 (95% CI: 1.93 - 3.67) for mortality and 2.04 (95% CI: 1.49 - 2.80) for poor functional outcome. Adjusted estimates indicated an OR of 1.22 (95% CI: 1.1 - 1.35) for mortality and 1.21 (95% CI: 1.04 - 1.41) for poor functional outcome, with substantial heterogeneity for both adjusted and unadjusted analyses. No publication bias was detected for the prevalence of frailty. However, there was a publication bias for the association between frailty and mortality. Conclusions: Frailty was significantly associated with increased mortality and poorer functional outcomes in stroke patients. Our study highlights the need to focus on frailty in stroke patients to improve outcomes and quality of life. Further research should aim to standardize assessment of frailty and reduce heterogeneity in study outcomes. Systematic review registration: https://www.crd.york.ac.uk/prospero/#searchadvanced, CRD42023470325.

Interventricular septum involvement is related to right ventricular dysfunction in anterior STEMI patients without right ventricular infarction: a cardiovascular magnetic resonance study.

The value of cardiovascular magnetic resonance (CMR) in assessing and predicting acute right ventricular (RV) dysfunction in patients with anterior ST-segment elevation myocardial infarction (STEMI) remains ascertained. Eighty eight patients with anterior STEMI were prospectively recruited and underwent CMR examinations within one week following the coronary intervention. Patients with RV ejection fraction (RVEF) less than 2 standard deviations below the average at the center (RVEF ≤ 45.0%) were defined as having RV dysfunction. The size of infarction, segmental wall motion, and T1 and T2 mapping values of global myocardium and the interventricular septum (IVS) were measured. Predictive performance was calculated using receiver-operating characteristic curve analysis and logistic regression test. Twenty two patients presented with RV dysfunction. The RV dysfunction group had a larger IVS infarct extent (54.28 ± 10.35 vs 33.95 ± 15.09%, P < 0.001) and lower left ventricle stroke volume index (33.93 ± 7.96 vs 42.46 ± 8.14 ml/m2, P < 0.001) compared to the non-RV dysfunction group. IVS infarct extent at 48.8% best predicted the presence of RV dysfunction with an area under the curve of 0.864. Left ventricular stroke volume index (LVSVI) and IVS infarct extent were selected by stepwise multivariable logistic regression analysis. Lower LVSVI (odds ratio [OR] 0.90; 95% confidence interval [CI], 0.79 to 0.99; P = 0.044) and higher IVS infarct extent (OR 1.16; 95% CI 1.05 to 1.33; P = 0.01) were found to be independent predictors for RV dysfunction. In patients with anterior STEMI, those with larger IVS infarct extent and worse LV function are more likely to be associated with RV dysfunction.

Wireless Magnetic Robot for Precise Hierarchical Control of Tissue Deformation.

Mechanotherapy has emerged as a promising treatment for tissue injury. However, existing robots for mechanotherapy are often designed on intuition, lack remote and wireless control, and have limited motion modes. Herein, through topology optimization and hybrid fabrication, wireless magneto-active soft robots are created that can achieve various modes of programmatic deformations under remote magnetic actuation and apply mechanical forces to tissues in a precise and predictable manner. These soft robots can quickly and wirelessly deform under magnetic actuation and are able to deliver compressing, stretching, shearing, and multimodal forces to the surrounding tissues. The design framework considers the hierarchical tissue-robot interaction and, therefore, can design customized soft robots for different types of tissues with varied mechanical properties. It is shown that these customized robots with different programmable motions can induce precise deformations of porcine muscle, liver, and heart tissues with excellent durability. The soft robots, the underlying design principles, and the fabrication approach provide a new avenue for developing next-generation mechanotherapy.

Unnatural lipids for simultaneous mRNA delivery and metabolic cell labeling.

Lipids have demonstrated tremendous promise for mRNA delivery, as evidenced by the success of Covid-19 mRNA vaccines. However, existing lipids are mostly used as delivery vehicles and lack the ability to monitor and further modulate the target cells. Here, for the first time, we report a class of unnatural lipids (azido-DOTAP) that can efficiently deliver mRNAs into cells and meanwhile metabolically label cells with unique chemical tags (e.g., azido groups). The azido tags expressed on the cell membrane enable the monitoring of transfected cells, and can mediate subsequent conjugation of cargos via efficient click chemistry for further modulation of transfected cells. We further demonstrate that the dual-functional unnatural lipid is applicable to different types of cells including dendritic cells, the prominent type of antigen presenting cells, potentially opening a new avenue to developing enhanced mRNA vaccines.

The influence of chlorination additives on metal separation during the pyrometallurgical recovery of spent lithium-ion batteries.

The difficulty of separating Li during pyrometallurgical smelting of spent lithium-ion batteries (LIBs) has limited the development of pyrometallurgical processes. Chlorination enables the conversion of Li from spent LIBs to the gas phase during the smelting process. In this paper, the effects of four solid chlorinating agents (KCl, NaCl, CaCl2 and MgCl2) on Li volatilization and metal (Co, Cu, Ni and Fe) recovery were investigated. The four solid chlorinating agents were systematically compared in terms of the direct chlorination capacities, indirect chlorination capacities, alloy physical losses and chemical losses in the slag. CaCl2 was better suited for use as a solid chlorinating agent to promote Li volatilization due to its excellent results in these indexes. The temperature required for the release of HCl from MgCl2, facilitated by CO2 and SiO2, was lower than 500 °C. The prematurely released HCl failed to participate in the chlorination reaction. This resulted in approximately 12 % less Li volatilization when MgCl2 was used as a chlorinating agent compared to when CaCl2 was used. In addition, the use of KCl as a chlorinating agent decreased the chemical dissolution loss of alloys in the slag. The performance of NaCl was mediocre. Finally, based on evaluations of the four indexes, recommendations for the selection and optimization of solid chlorinating agents were provided.

Five years of change in adult twins: longitudinal changes of genetic and environmental influence on epigenetic clocks.

BACKGROUND: Epigenetic clocks were known as promising biomarkers of aging, including original clocks trained by individual CpG sites and principal component (PC) clocks trained by PCs of CpG sites. The effects of genetic and environmental factors on epigenetic clocks are still unclear, especially for PC clocks. METHODS: We constructed univariate twin models in 477 same-sex twin pairs from the Chinese National Twin Registry (CNTR) to estimate the heritability of five epigenetic clocks (GrimAge, PhenoAge, DunedinPACE, PCGrimAge, and PCPhenoAge). Besides, we investigated the longitudinal changes of genetic and environmental influences on epigenetic clocks across 5 years in 134 same-sex twin pairs. RESULTS: Heritability of epigenetic clocks ranged from 0.45 to 0.70, and those for PC clocks were higher than those for original clocks. For five epigenetic clocks, the longitudinal stability was moderate to high and was largely due to genetic effects. The genetic correlations between baseline and follow-up epigenetic clocks were moderate to high. Special unique environmental factors emerged both at baseline and at follow-up. PC clocks showed higher longitudinal stability and unique environmental correlations than original clocks. CONCLUSIONS: For five epigenetic clocks, they have the potential to identify aging interventions. High longitudinal stability is mainly due to genetic factors, and changes of epigenetic clocks over time are primarily due to changes in unique environmental factors. Given the disparities in genetic and environmental factors as well as longitudinal stability between PC and original clocks, the results of studies with original clocks need to be further verified with PC clocks.

Mitochondrial dysfunction-associated alveolar epithelial senescence is involved in CdCl2-induced COPD-like lung injury.

An earlier study found that respiratory cadmium chloride (CdCl2) exposure caused COPD-like lung injury. This study aimed to explore whether mitochondrial dysfunction-mediated alveolar epithelial senescence is involved in CdCl2-induced COPD-like lung injury. Adult C57BL/6 mice were exposed to CdCl2 (10 mg/L) aerosol for six months. Beta-galactosidase-positive cells, p21 and p16 were increased in CdCl2-exposed mouse lungs. The in vitro experiments showed that γ-H2AX was elevated in CdCl2-exposed alveolar epithelial cells. The cGAS-STING pathway was activated in CdCl2-exposed alveolar epithelial cells and mouse lungs. Cxcl1, Cxcl9, Il-10, Il-1ß and Mmp2, several senescence-associated secretory phenotypes (SASP), were upregulated in CdCl2-exposed alveolar epithelial cells. Mechanistically, CdCl2 exposure caused SIRT3 reduction and mitochondrial dysfunction in mouse lungs and alveolar epithelial cells. The in vitro experiment found that Sirt3 overexpression attenuated CdCl2-induced alveolar epithelial senescence and SASP. The in vivo experiments showed that Sirt3 gene knockout exacerbated CdCl2-induced alveolar epithelial senescence, alveolar structure damage, airway inflammation and pulmonary function decline. NMN, an NAD+ precursor, attenuated CdCl2-induced alveolar epithelial senescence and SASP in mouse lungs. Moreover, NMN supplementation prevented CdCl2-induced COPD-like alveolar structure damage, epithelial-mesenchymal transition and pulmonary function decline. These results suggest that mitochondrial dysfunction-associated alveolar epithelial senescence is involved in CdCl2-induced COPD-like lung injury.