Circular RNA IGF1R Promotes Cardiac Repair via Activating ß-Catenin Signaling by Interacting with DDX5 in Mice after Ischemic Insults.

The potential of circular RNAs (circRNAs) as biomarkers and therapeutic targets is becoming increasingly evident, yet their roles in cardiac regeneration and myocardial renewal remain largely unexplored. Here, we investigated the function of circIGF1R and related mechanisms in cardiac regeneration. Through analysis of circRNA sequencing data from neonatal and adult cardiomyocytes, circRNAs associated with regeneration were identified. Our data showed that circIGF1R expression was high in neonatal hearts, decreased with postnatal maturation, and up-regulated after cardiac injury. The elevation was validated in patients diagnosed with acute myocardial infarction (MI) within 1 week. In human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) and myocardial tissue from mice after apical resection and MI, we observed that circIGF1R overexpression enhanced cardiomyocyte proliferation, reduced apoptosis, and mitigated cardiac dysfunction and fibrosis, while circIGF1R knockdown impeded endogenous cardiac renewal. Mechanistically, we identified circIGF1R binding proteins through circRNA precipitation followed by mass spectrometry. RNA pull-down Western blot and RNA immunoprecipitation demonstrated that circIGF1R directly interacted with DDX5 and augmented its protein level by suppressing ubiquitin-dependent degradation. This subsequently triggered the ß-catenin signaling pathway, leading to the transcriptional activation of cyclin D1 and c-Myc. The roles of circIGF1R and DDX5 in cardiac regeneration were further substantiated through site-directed mutagenesis and rescue experiments. In conclusion, our study highlights the pivotal role of circIGF1R in facilitating heart regeneration and repair after ischemic insults. The circIGF1R/DDX5/ß-catenin axis emerges as a novel therapeutic target for enhancing myocardial repair after MI, offering promising avenues for the development of regenerative therapies.

Room-Temperature Liquid Crystalline Tetraphenylethylene-Surfactant Complex with Chiral Supramolecular Structure and Tunable Circularly Polarized Luminescence.

A novel room-temperature liquid crystal of tetraphenylethylene derivative (TPE-DHAB) was synthesized using an ionic self-assembly strategy. The TPE-DHAB complex exhibits typical aggregation-induced emission properties and a unique helical supramolecular structure. Moreover, the generation and handedness inversion of circularly polarized luminescence (CPL) can be achieved through further chiral solvation, providing a facile approach to fabricate room-temperature liquid crystalline materials with controllable supramolecular structures and tunable CPL properties through a synergistic strategy of ionic self-assembly and chiral solvation process.

Initial Litter Chemistry and UV Radiation Drive Chemical Divergence in Litter during Decomposition.

Litter's chemical complexity influences carbon (C) cycling during its decomposition. However, the chemical and microbial mechanisms underlying the divergence or convergence of chemical complexity under UV radiation remain poorly understood. Here, we conducted a 397-day field experiment using 13C cross-polarization magic-angle spinning nuclear magnetic resonance (13C-CPMAS NMR) to investigate the interactions among the initial chemistry, microbial communities, and UV radiation during decomposition. Our study found that the initial concentrations of O-substituted aromatic C, di-O-alkyl C, and O-alkyl C in Deschampsia caespitosa were higher than those in Kobresia tibetica. Litter's chemical composition exhibited divergent patterns based on the initial chemistry, UV radiation, and decay time. Specifically, D. caespitosa consistently displayed higher concentrations of di-O-alkyl C and O-alkyl C compared to K. tibetica, regardless of the UV exposure and decay time. Additionally, litter's chemical complexity was positively correlated with changes in the extracellular enzyme activities, particularly those involved in lignin, cellulose, and hemicellulose degradation, which accounted for 9%, 20%, and 4% of the variation in litter's chemical complexity, respectively. These findings highlighted the role of distinct microbial communities in decomposing different C components through catabolism, leading to chemical divergence in litter. During the early decomposition stages, oligotrophic Planctomycetes and Acidobacteria metabolized O-alkyl C and di-O-alkyl C under UV-blocking conditions. In contrast, copiotrophic Actinobacteria and Chytridiomycota utilized these components under UV radiation exposure, reflecting their ability to thrive under UV stress conditions due to their rapid growth strategies in environments rich in labile C. Our study revealed that the inherent differences in the initial O-alkyl C and di-O-alkyl C contributed to the chemical divergence, while UV radiation further influenced this divergence by shifting the microbial community composition from oligotrophic to copiotrophic species. Thus, differences in the initial litter chemistry, microbial community, and UV radiation affected the quantity and quality of plant-derived C during decomposition.

Interleukin-33 links asthma to alopecia areata: Mendelian randomization and mediation analysis.

OBJECTIVE: The objective of this study is to elucidate the causal association between asthma and alopecia areata (AA) through the application of Mendelian randomization (MR) analysis, leveraging summary data from genome-wide association studies (GWAS). Additionally, it explores potential mediating factors. MATERIALS AND METHODS: Mendelian randomization (MR) analysis was employed to investigate the causal relationship between asthma and AA using genetic instrumental variables (IVs) for asthma, 91 circulating inflammatory proteins, and AA extracted from large-scale GWAS. The primary analytical approach utilized the inverse-variance weighted (IVW) method, supplemented by weighted median and MR-Egger methods to assess robustness. Tests for heterogeneity and pleiotropy were conducted to ensure result reliability. Furthermore, the study examined the mediating role of circulating inflammatory proteins in the asthma-AA relationship. RESULTS: The findings revealed an increased risk of AA among asthma patients (odds ratio (OR) = 14.070; 95% confidence interval (CI) = 1.410-140.435; P = 0.024). Interleukin-33 (IL-33) emerged as a significant mediator in the asthma-AA relationship, explaining 13.1% of the mediation effect. Bidirectional Mendelian randomization analyses did not establish a causal effect of AA on asthma occurrence. CONCLUSION: This study, utilizing Mendelian Randomization, elucidates the causal link between asthma and AA, highlighting the mediating role of IL-33. These findings underscore the importance of considering AA risk in asthma management and offer insights for potential therapeutic strategies targeting IL-33. Future research should explore additional biomarkers and mediating mechanisms between asthma and AA to enhance treatment approaches and patient quality of life.

PEX3 promotes regenerative repair after myocardial injury in mice through facilitating plasma membrane localization of ITGB3.

The peroxisome is a versatile organelle that performs diverse metabolic functions. PEX3, a critical regulator of the peroxisome, participates in various biological processes associated with the peroxisome. Whether PEX3 is involved in peroxisome-related redox homeostasis and myocardial regenerative repair remains elusive. We investigate that cardiomyocyte-specific PEX3 knockout (Pex3-KO) results in an imbalance of redox homeostasis and disrupts the endogenous proliferation/development at different times and spatial locations. Using Pex3-KO mice and myocardium-targeted intervention approaches, the effects of PEX3 on myocardial regenerative repair during both physiological and pathological stages are explored. Mechanistically, lipid metabolomics reveals that PEX3 promotes myocardial regenerative repair by affecting plasmalogen metabolism. Further, we find that PEX3-regulated plasmalogen activates the AKT/GSK3ß signaling pathway via the plasma membrane localization of ITGB3. Our study indicates that PEX3 may represent a novel therapeutic target for myocardial regenerative repair following injury.

Checkpoint Kinase 1 Stimulates Endogenous Cardiomyocyte Renewal and Cardiac Repair by Binding to Pyruvate Kinase Isoform M2 C-Domain and Activating Cardiac Metabolic Reprogramming in a Porcine Model of Myocardial Ischemia/Reperfusion Injury.

BACKGROUND: The regenerative capacity of the adult mammalian hearts is limited. Numerous studies have explored mechanisms of adult cardiomyocyte cell-cycle withdrawal. This translational study evaluated the effects and underlying mechanism of rhCHK1 (recombinant human checkpoint kinase 1) on the survival and proliferation of cardiomyocyte and myocardial repair after ischemia/reperfusion injury in swine. METHODS AND RESULTS: Intramyocardial injection of rhCHK1 protein (1 mg/kg) encapsulated in hydrogel stimulated cardiomyocyte proliferation and reduced cardiac inflammation response at 3 days after ischemia/reperfusion injury, improved cardiac function and attenuated ventricular remodeling, and reduced the infarct area at 28 days after ischemia/reperfusion injury. Mechanistically, multiomics sequencing analysis demonstrated enrichment of glycolysis and mTOR (mammalian target of rapamycin) pathways after rhCHK1 treatment. Co-Immunoprecipitation (Co-IP) experiments and protein docking prediction showed that CHK1 (checkpoint kinase 1) directly bound to and activated the Serine 37 (S37) and Tyrosine 105 (Y105) sites of PKM2 (pyruvate kinase isoform M2) to promote metabolic reprogramming. We further constructed plasmids that knocked out different CHK1 and PKM2 amino acid domains and transfected them into Human Embryonic Kidney 293T (HEK293T) cells for CO-IP experiments. Results showed that the 1-265 domain of CHK1 directly binds to the 157-400 amino acids of PKM2. Furthermore, hiPSC-CM (human iPS cell-derived cardiomyocyte) in vitro and in vivo experiments both demonstrated that CHK1 stimulated cardiomyocytes renewal and cardiac repair by activating PKM2 C-domain-mediated cardiac metabolic reprogramming. CONCLUSIONS: This study demonstrates that the 1-265 amino acid domain of CHK1 binds to the 157-400 domain of PKM2 and activates PKM2-mediated metabolic reprogramming to promote cardiomyocyte proliferation and myocardial repair after ischemia/reperfusion injury in adult pigs.

Phase tracking using a Kalman filter based on probability density distribution in frequency-scanning interferometry.

Frequency-scanning interferometry (FSI) utilizing external cavity diode lasers (ECDL) stands out as a potent technique for absolute distance measurement. Nevertheless, the inherent scanning nonlinearity of ECDL and phase noise pose a challenge, as it can compromise the accuracy of phase extraction from interference signals, thereby reducing the measurement accuracy of FSI. In this study, we propose a composite algorithm aimed at mitigating non-orthogonal errors by integrating the least-squares and Heydemann correction technique. Furthermore, we employ Kalman filtering for precise phase tracking. We introduce a parameter selection strategy based on the statistical distribution of instantaneous frequency to achieve the fusion estimation of phase observation values and theoretical models, which starts a new perspective for the application of multi-dimensional data fusion in FSI measurement. Through simulation and experimental validation, the efficacy of this approach is confirmed. The experimental results show promising outcomes: with an average phase error of 0.12%, a standard deviation of less than 1.7 µm in absolute distance measurement, and an average positioning accuracy error of 0.29 µm.

Initial microbiome and tree root status structured the soil microbial community discrepancy of the subtropical pine-oak forest in a large urban forest park.

Plant-microbe-soil interactions control over the forest biogeochemical cycling. Adaptive plant-soil interactions can shape specific microbial taxa in determining the ecosystem functioning. Different trees produce heterogeneous soil properties and can alter the composition of soil microbial community, which is relevant to the forest internal succession containing contrasting stand types such as the pine-oak forests. Considering representative microbial community characteristics are recorded in the original soil where they had adapted and resided, we constructed a soil transplant incubation experiment in a series of in situ root-ingrowth cores in a subtropical pine-oak forest, to simulate the vegetational pine-oak replacement under environmental succession. The responsive bacterial and fungal community discrepancies were studied to determine whether and how they would be changed. The pine and oak forest stands had greater heterogeneity in fungi composition than bacteria. Original soil and specific tree root status were the main factors that determined microbial community structure. Internal association network characters and intergroup variations of fungi among soil samples were more affected by original soil, while bacteria were more affected by receiving forest. Specifically, dominant tree roots had strong influence in accelerating the fungi community succession to adapt with the surrounding forest. We concluded that soil microbial responses to forest stand alternation differed between microbiome groups, with fungi from their original forest possessing higher resistance to encounter a new vegetation stand, while the bacteria community have faster resilience. The data would advance our insight into local soil microbial community dynamics during ecosystem succession and be helpful to enlighten forest management.

Distribution patterns and environmental risk assessments of microplastics in the lake waters and sediments from eight typical wetland parks in Changsha city, China.

The quality of water in urban parks is closely related to people's daily lives, but the pollution caused by microplastics in park water and sediments has not been comprehensively studied. Therefore, eight typical parks in the urban area of Changsha, China, were selected, and Raman spectroscopy was used to explore the spatial distributions and compositions of the microplastics in the water and sediments, analyze their influencing factors, and evaluate their environmental risks. The results showed that the abundances of surface water microplastics in all parks ranged from 150 to 525 n L-1, and the abundances of sediment microplastics ranged from 120 to 585 n kg-1. The microplastics in the surface water included polyethylene terephthalate (PET), chlorinated polyethylene (CPE), and fluororubber (FLU), while those in the sediments included polyvinyl chloride (PVC), wp-acrylate copolymer (ACR), and CPE. Regression analyses revealed significant positive correlations between human activities and the abundances of microplastics in the parks. Among them, the correlations of population, industrial discharge and domestic wastewater discharge with the abundance of microplastics in park water were the strongest. However, the correlations of car flow and tourists with the abundance of microplastics in park water were the weakest. Based on the potential ecological risk indices (PERI) classification assessment method, the levels of microplastics in the waters and sediments of the eight parks were all within the II-level risk zone (53-8,549), among which the risk indices for Meixi Lake and Yudai Lake were within the IV risk zone (1,365-8,549), which may have been caused by the high population density near the park. This study provides new insights into the characteristics of microplastics in urban park water and sediment.

The Application of "Table Tennis Racquet" Random Skin Flap in the Treatment of Facial Skin Carcinoma.

BACKGROUND: The repair of facial skin and soft tissue defects remains a clinical challenge. The author introduced a novel "table tennis racquet" random skin flap for wound repair after facial skin cancer excision and discussed its survival mechanisms. METHODS: A lateral mandibular neck skin flap shaped like a table tennis racquet with no well-known blood vessels at the narrow pedicle was designed in 31 cases to repair tissue defects. Among them, there were 8 cases of skin carcinoma in the frontotemporal area and 23 cases of skin carcinoma in the cheek. The flap area was 8.0 × 7.0 cm at maximum and 3.0 × 2.5 cm at minimum, with a pedicle width of 1.0-2.0 cm and a pedicle length of 2.0-6.0 cm. RESULTS: All 31 "table tennis racquet" random skin flaps survived, although there were 3 cases with delayed healing of distal flap bruising. All of them had an ideal local shape after repair with a concealed donor area and inconspicuous scars. CONCLUSIONS: This flap has a "table tennis racquet" shape with a pedicle without well-known blood vessels and has a length-to-width ratio that exceeds that of conventional random flaps, making it unconventional. Because of its long and narrow pedicle, it not only has a large rotation and coverage area but also can be designed away from the defect area, avoiding the defect of no donor tissue being localized near the defect. Overall, this approach is an ideal option for repairing tissue defects after enlarged excision of facial skin carcinoma.

Symptom-to-balloon time and risk of ventricular arrhythmias in patients with STEMI undergoing percutaneous coronary intervention: The VERY-STEMI study.

Background: Ventricular arrhythmias (VAs) mainly occur in the early post-myocardial infarction (MI) period. However, studies examining the association between total myocardial ischemia time interval and the risk of new-onset VAs during a long-term follow-up are scarce. Methods: This study (symptom-to-balloon time and VEntricular aRrhYthmias in patients with STEMI, VERY-STEMI study) was a multicenter, observational cohort and real-world study, which included patients with ST-segment elevation MI (STEMI) undergoing percutaneous coronary intervention (PCI). The primary endpoint was cumulative new-onset VAs during follow-up. The secondary endpoints were the major adverse cardiovascular events (MACE) and changes in left ventricular ejection fraction (ΔLVEF, %). Results: A total of 517 patients with STEMI were included and 236 primary endpoint events occurred. After multivariable adjustments, compared to patients with S2BT of 24 h-7d, those with S2BT ≤ 24 h and S2BT > 7d had a lower risk of primary endpoint. RCS showed an inverted U-shaped relationship between S2BT and the primary endpoint, with an S2BT of 68.4 h at the inflection point. Patients with S2BT ≤ 24 h were associated with a lower risk of MACE and a 4.44 increase in LVEF, while there was no significant difference in MACE and LVEF change between the S2BT > 7d group and S2BT of 24 h-7d group. Conclusions: S2BT of 24 h-7d in STEMI patients was associated with a higher risk of VAs during follow-up. There was an inverted U-shaped relationship between S2BT and VAs, with the highest risk at an S2BT of 68.4 h.

Mitochondrial stress response and myogenic differentiation.

Regeneration and repair are prerequisites for maintaining effective function of skeletal muscle under high energy demands, and myogenic differentiation is one of the key steps in the regeneration and repair process. A striking feature of the process of myogenic differentiation is the alteration of mitochondria in number and function. Mitochondrial dysfunction can activate a number of transcriptional, translational and post-translational programmes and pathways to maintain cellular homeostasis under different types and degrees of stress, either through its own signaling or through constant signaling interactions with the nucleus and cytoplasm, a process known as the mitochondrial stress responses (MSRs). It is now believed that mitochondrial dysfunction is closely associated with a variety of muscle diseases caused by reduced levels of myogenic differentiation, suggesting the possibility that MSRs are involved in messaging during myogenic differentiation. Also, MSRs may be involved in myogenesis by promoting bioenergetic remodeling and assisting myoblast survival during myogenic differentiation. In this review, we will take MSRs as an entry point to explore its concrete regulatory mechanisms during myogenic differentiation, with a perspective to provide a theoretical basis for the treatment and repair of related muscle diseases.

Functional characterization of Helicoverpa assulta CYP6B6 in insecticide metabolism.

The oriental tobacco budworm Helicoverpa assulta (Lepidoptera: Noctuidae) is a specialist pest that may cause serious damages to important crops such as chili pepper and tobacco. Various man-made insecticides have been applied to control the infestation of this pest. To understand how this pest copes with insecticides, it is required to identify key players involved in insecticide transformation. In this study, a P450 gene of CYP6B subfamily was identified in the oriental tobacco budworm, and its expression pattern was revealed. Moreover, the activities of HassCYP6B6 against 12 insecticides were explored using recombinant enzymes produced in the facile Escherichia coli. Data from metabolic experiments showed that HassCYP6B6 was able to metabolize conventional insecticides including organophosporates (diazinon, malathion, phoxim), carbamate propoxur, and pyrethroid esfenvalerate, while no significant metabolism was observed towards new-type pesticides such as neonicotinoids (acetamiprid, imidacloprid), diamides (chlorantraniliprole, cyantraniliprole), macrocyclic lactone (emamectin benzoate, ivermectin), and metaflumizone. Structures of metabolites were proposed based on mass spectrometry analyses. The results demonstrate that HassCYP6B6 plays important roles in the transformation of multiple insecticides via substrate-dependent catalytic mechanisms including dehydrogenation, hydroxylation and oxidative desulfurization. The findings have important applied implications for the usage of insecticides.

Synchronous filtering method for improving the optical signal-to-noise ratio of a tunable laser based on the Fabry-Pérot interferometer.

Optical measurements are closely related to the optical signal-to-noise ratio (OSNR) of the laser, which can be improved using a tunable optical filter (TOF) to suppress frequency noise. For an external-cavity tunable laser with a tuning range larger than the TOF bandwidth, the wavelength at the center of the TOF passband must be varied based on the laser tuning. This study proposes a tunable-laser OSNR-enhancement method based on the Fabry-Pérot (FP) interferometer. The FP signal contains the wavelength information of the swept laser, which can be used to determine the real-time driving voltage of the TOF. Notably, the laser needs to be continuously tunable without mode hopping, and the free spectral range of the FP interferometer must be smaller than the TOF bandwidth.

The role and regulation of SIRT1 in pulmonary fibrosis.

Pulmonary fibrosis (PF) is a progressive and fatal lung disease with high incidence and a lack of effective treatment, which is a severe public health problem. PF has caused a huge socio-economic burden, and its pathogenesis has become a research hotspot. SIRT1 is a nicotinamide adenosine dinucleotide (NAD)-dependent sirtuin essential in tumours, Epithelial mesenchymal transition (EMT), and anti-aging. Numerous studies have demonstrated after extensive research that it is crucial in preventing the progression of pulmonary fibrosis. This article reviews the biological roles and mechanisms of SIRT1 in regulating the progression of pulmonary fibrosis in terms of EMT, oxidative stress, inflammation, aging, autophagy, and discusses the potential of SIRT1 as a therapeutic target for pulmonary fibrosis, and provides a new perspective on therapeutic drugs and prognosis prospects.

Reticulocyte hemoglobin content associated with the risk of iron deficiency anemia.

Background/Objective: Reticulocyte hemoglobin content (MCHr) was recognized as a rapid and reliable marker for investigating iron deficiency (ID). We hypothesized that MCHr was associated with the risk of iron deficiency anemia in adults. Methods: This is a dual-center case-control study. A total of 806 patients and healthy individuals were recruited from Ruijin Hospital and Xinhua Hospital affiliated to Shanghai Jiaotong University School of Medicine between January 2021 and December 2021. The participants were categorized into iron deficiency anemia (IDA) group (n = 302), non-IDA group (n = 366), and healthy control group (n = 138). According to the MCHr level, the participants were divided into two groups, i.e. normal MCHr (≥25 pg) and decreased MCHr (<25 pg) group. Multivariate logistic regression analysis and adjusted subgroup analysis were conducted to estimate the relative risk between MCHr and IDA, with confounding factors including age, sex, hemoglobin (Hb), mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC), Hematocrit (HCT), serum iron (Fe), ferritin (Ferrit), and total iron binding capacity (TIBC). Results: Compared with the non-IDA, the MCHr level with IDA decreased significantly. ROC curve analysis showed that MCHr had the largest area under the AUC curve. After comprehensive adjustment for confounding factors, individuals with normal level of MCHr exhibited a decreased risk of IDA (OR = 0.68 [0.60, 0.77], P < 0.01), while the risk of IDA was up to 5 times higher for those with decreased MCHr. Conclusion: Our findings supported the hypothesis that MCHr was associated with the risk of IDA in adults and could serve as an indicator of IDA severity. MCHr holds clinical value as an auxiliary diagnostic indicator, providing valuable insights into whether invasive examinations are warranted in the assessment of IDA.

Multiple factors interact in editing of PPR-E+-targeted sites in maize mitochondria and plastids.

RNA cytidine-to-uridine editing is essential for plant organellar gene expression. Pentatricopeptide repeat (PPR)-E+ proteins have been proposed to bind to target sites and recruit the cytidine deaminase AtDYW2, facilitated by AtNUWA. Here we analyze the function of ZmNUWA, ZmDYW2A, and ZmDYW2B and their relationships with other editing factors in maize. The zmdyw2a and zmdyw2b single mutants are normal, but the zmdyw2a::zmdyw2b and zmnuwa mutants are severely arrested in seed development. ZmNUWA, ZmDYW2A, and ZmDYW2B are dual localized in mitochondria and plastids. Loss of ZmNUWA decreases the editing at 99 mitochondrial sites and 8 plastid sites. Surprisingly, loss of ZmDYW2A:ZmDYW2B affects almost the same set of sites targeted by PPR-E+ proteins. ZmNUWA interacts with ZmDYW2A and ZmDYW2B, suggesting that ZmNUWA recruits ZmDYW2A/2B in the editing of PPR-E+-targeted sites in maize. Further protein interaction analyses show that ZmNUWA and ZmDYW2A/2B interact with ZmMORF1, ZmMORF8, ZmMORF2, and ZmMORF9 and that ZmOZ1 interacts with ZmORRM1, ZmDYW2A, ZmDYW2B, ZmMORF8, and ZmMORF9. These results suggest that the maize mitochondrial PPR-E+ editosome contains PPR-E+, ZmDYW2A/2B, ZmNUWA, and ZmMORF1/8, whereas the plastid PPR-E+ editosome is composed of PPR-E+, ZmDYW2A/2B, ZmNUWA, ZmMORF2/8/9, ZmORRM1, and ZmOZ1.

Anoikis-related CTNND1 is associated with immuno-suppressive tumor microenvironment and predicts unfavorable immunotherapeutic outcome in non-small cell lung cancer.

Background: Immunotherapy has greatly changed the treatment of advanced non-small cell lung cancer (NSCLC). Anoikis is a programmed cell death process associated with cancer. However, the correlation between anoikis-related genes and the tumor microenvironment (TME) features and immunotherapeutic outcome in NSCLC has not been fully explored. Methods: The bulk and single-cell transcriptome data of NSCLC were downloaded from TCGA and GEO databases. The distribution of anoikis-related genes on different cell types at the single-cell level was analyzed, and these genes specifically expressed by tumor cells and immunotherapy-related were further extracted. Next, the candidate gene CTNND1 was identified and its correlations with the TME features and immunotherapeutic outcome in NSCLC were explored in multiple public cohorts. Finally, an in-house cohort was used to determine the CTNND1 expression and immuno-correlation in NSCLC. Results: At single-cell atlas, we found that anoikis-related genes expressed specifically in tumor cells of NSCLC. By intersecting anoikis-related genes, immunotherapy-associated genes, and the genes expressed in tumor cells, we obtained a special biomarker CTNND1. In addition, cell-cell communication analysis revealed that CTNND1+ tumor cells communicated with immune subpopulations frequently. Moreover, we found that high expression of CTNND1 was related to immuno-suppressive status of NSCLC. The expression of CTNND1 and its immuno-correlation were also validated, and the results showed that CTNND1 was highly expressed in NSCLC tissues and tumors with high CTNND1 expression accompanied with low CD8+ T cells infiltration. Conclusions: Overall, our study reported that CTNND1 can be considered as a novel biomarker for the predication of immunotherapeutic responses and a potential target for NSCLC therapy.

LncRNA-mediated Modulation of Endothelial Cells: Novel Progress in the Pathogenesis of Coronary Atherosclerotic Disease.

Coronary atherosclerotic disease (CAD) is a common cardiovascular disease and an important cause of death. Moreover, endothelial cells (ECs) injury is an early pathophysiological feature of CAD, and long noncoding RNAs (lncRNAs) can modulate gene expression. Recent studies have shown that lncRNAs are involved in the pathogenesis of CAD, especially by regulating ECs. In this review, we summarize the novel progress of lncRNA-modulated ECs in the pathogenesis of CAD, including ECs proliferation, migration, adhesion, angiogenesis, inflammation, apoptosis, autophagy, and pyroptosis. Thus, as lncRNAs regulate ECs in CAD, lncRNAs will provide ideal and novel targets for the diagnosis and drug therapy of CAD.