Regulation of Keap1-Nrf2 signaling in health and diseases.

Nuclear factor erythroid 2-related factor 2 (Nrf2) functions as a central regulator in modulating the activities of diverse antioxidant enzymes, maintaining cellular redox balance, and responding to oxidative stress (OS). Kelch-like ECH-associated protein 1 (Keap1) serves as a principal negative modulator in controlling the expression of detoxification and antioxidant genes. It is widely accepted that OS plays a pivotal role in the pathogenesis of various diseases. When OS occurs, leading to inflammatory infiltration of neutrophils, increased secretion of proteases, and the generation of large quantities of reactive oxygen radicals (ROS). These ROS can oxidize or disrupt DNA, lipids, and proteins either directly or indirectly. They also cause gene mutations, lipid peroxidation, and protein denaturation, all of which can result in disease. The Keap1-Nrf2 signaling pathway regulates the balance between oxidants and antioxidants in vivo, maintains the stability of the intracellular environment, and promotes cell growth and repair. However, the antioxidant properties of the Keap1-Nrf2 signaling pathway are reduced in disease. This review overviews the mechanisms of OS generation, the biological properties of Keap1-Nrf2, and the regulatory role of its pathway in health and disease, to explore therapeutic strategies for the Keap1-Nrf2 signaling pathway in different diseases.

Assessment of left ventricular ejection fraction in artificial intelligence based on left ventricular opacification.

Background: Left ventricular opacification (LVO) improves the accuracy of left ventricular ejection fraction (LVEF) by enhancing the visualization of the endocardium. Manual delineation of the endocardium by sonographers has observer variability. Artificial intelligence (AI) has the potential to improve the reproducibility of LVO to assess LVEF. Objectives: The aim was to develop an AI model and evaluate the feasibility and reproducibility of LVO in the assessment of LVEF. Methods: This retrospective study included 1305 echocardiography of 797 patients who had LVO at the Department of Ultrasound Medicine, Union Hospital, Huazhong University of Science and Technology from 2013 to 2021. The AI model was developed by 5-fold cross validation. The validation datasets included 50 patients prospectively collected in our center and 42 patients retrospectively collected in the external institution. To evaluate the differences between LV function determined by AI and sonographers, the median absolute error (MAE), spearman correlation coefficient, and intraclass correlation coefficient (ICC) were calculated. Results: In LVO, the MAE of LVEF between AI and manual measurements was 2.6% in the development cohort, 2.5% in the internal validation cohort, and 2.7% in the external validation cohort. Compared with two-dimensional echocardiography (2DE), the left ventricular (LV) volumes and LVEF of LVO measured by AI correlated significantly with manual measurements. AI model provided excellent reliability for the LV parameters of LVO (ICC > 0.95). Conclusions: AI-assisted LVO enables more accurate identification of the LV endocardium and reduces observer variability, providing a more reliable way for assessing LV function.

Microbial community interactions determine the mineralization of soil organic phosphorus in subtropical forest ecosystems.

In subtropical forest ecosystems with few phosphorus (P) inputs, P availability and forest productivity depend on soil organic P (Po) mineralization. However, the mechanisms by which the microbial community determines the status and fate of soil Po mineralization remain unclear. In the present study, soils were collected from three typical forest types: secondary natural forest (SNF), mixed planting, and monoculture forest of Chinese fir. The P fractions, Po-mineralization ability, and microbial community in the soils of different forest types were characterized. In addition, we defined Po-mineralizing taxa with the potential to interact with the soil microbial community to regulate Po mineralization. We found that a higher labile P content persisted in SNF and was positively associated with the Po-mineralization capacity of the soil microbial community. In vitro cultures of soil suspensions revealed that soil Po mineralization of three forest types was distinguished by differences in the composition of fungal communities. We further identified broad phylogenetic lineages of Po-mineralizing fungi with a high intensity of positive interactions with the soil microbial community, implying that the facilitation of Po-mineralizing taxa is crucial for soil P availability. Our dilution experiments to weaken microbial interactions revealed that in SNF soil, which had the highest interaction intensity of Po-mineralizing taxa with the community, Po-mineralization capacity was irreversibly lost after dilution, highlighting the importance of microbial diversity protection in forest soils. In summary, this study demonstrates that the interactions of Po-mineralizing microorganisms with the soil microbial community are critical for P availability in subtropical forests.IMPORTANCEIn subtropical forest ecosystems with few phosphorus inputs, phosphorus availability and forest productivity depend on soil organic phosphorus mineralization. However, the mechanisms by which the microbial community interactions determine the mineralization of soil organic phosphorus remain unclear. In the present study, soils were collected from three typical forest types: secondary natural forest, mixed planting, and monoculture forest of Chinese fir. We found that a higher soil labile phosphorus content was positively associated with the organic phosphorus mineralization capacity of the soil microbial community. Soil organic phosphorus mineralization of three forest types was distinguished by the differences in the composition of fungal communities. The positive interactions between organic phosphorus-mineralizing fungi and the rest of the soil microbial community facilitated organic phosphorus mineralization. This study highlights the importance of microbial diversity protection in forest soils and reveals the microbial mechanism of phosphorus availability maintenance in subtropical forest ecosystems.

Ferritinophagy-mediated ferroptosis facilitates methotrexate-induced hepatotoxicity by high-mobility group box 1 (HMGB1).

BACKGROUND AND AIM: Hepatotoxicity is a well-defined reaction to methotrexate (MTX), a drug commonly used for the treatment of rheumatoid arthritis and various tumours. We sought to elucidate the mechanism underlying MTX-induced hepatotoxicity and establish a potentially effective intervention strategy. METHODS: We administered MTX to liver cells and mice and assessed hepatotoxicity by cell viability assay and hepatic pathological changes. We determined ferroptosis and ferritinophagy by detecting ferroptosis-related markers and autophagic degradation of ferritin heavy chain 1 (FTH1). RESULTS: We have shown that hepatocytes treated with MTX undergo ferroptosis, and this process can be attenuated by ferroptosis inhibitors. Interestingly, NCOA4-mediated ferritinophagy was found to be involved in MTX-induced ferroptosis, which was demonstrated by the relief of ferroptosis through the inhibition of autophagy or knockdown of Ncoa4. Furthermore, MTX treatment resulted in the elevation of high-mobility group box 1 (HMGB1) expression. The depletion of Hmgb1 in hepatocytes considerably alleviated MTX-induced hepatotoxicity by limiting autophagy and the subsequent autophagy-dependent ferroptosis. It is noteworthy that glycyrrhizic acid (GA), a precise inhibitor of HMGB1, effectively suppressed autophagy, ferroptosis and hepatotoxicity caused by MTX. CONCLUSION: Our study shows the significant roles of autophagy-dependent ferroptosis and HMGB1 in MTX-induced hepatotoxicity. It emphasizes that the inhibition of ferritinophagy and HMGB1 may have potential as a therapeutic approach for preventing and treating MTX-induced liver injury.

Ultra-Broadband Flexible Thin-Film Sensor for Sound Monitoring and Ultrasonic Diagnosis.

Small-scale and flexible acoustic probes are more desirable for exquisite objects like human bodies and complex-shaped components than conventional rigid ones. Herein, a thin-film flexible acoustic sensor (FA-TES) that can detect ultra-broadband acoustic signals in multiple applications is proposed. The device consists of two thin copper-coated polyvinyl chloride films, which are stimulated by acoustic waves and contact each other to generate the triboelectric signal. Interlocking nanocolumn arrays fabricated on the friction surfaces are regarded as a highly adaptive spacer enabling this device to respond to ultra-broadband acoustic signals (100 Hz-4 MHz) and enhance sensor sensitivity for film weak vibration. Benefiting from the characteristics of high shape adaptability and ultrawide response range, the FA-TES can precisely sense human physiological sounds and voice (≤10 kHz) for laryngeal health monitoring and interaction in real-time. Moreover, the FA-TES flexibly arranged on a 3D-printed vertebra model can effectively and accurately diagnose the inner defect by ultrasonic testing (≥1 MHz). It envisions that this work can provide new ideas for flexible acoustic sensor designs and optimize real-time acoustic detections of human bodies and complex components.

Heme oxygenase-1: A potential therapeutic target for improving skeletal muscle atrophy.

Skeletal muscle atrophy is a common muscle disease that is directly caused by an imbalance in protein synthesis and degradation. At the histological level, it is mainly characterized by a reduction in muscle mass and fiber cross-sectional area (CSA). Patients with skeletal muscle atrophy present with reduced motor ability, easy fatigue, and poor life quality. Heme oxygenase-1 (HO-1) is an inducible enzyme that catalyzes the degradation of heme and has attracted much attention for its anti-oxidation effects. In addition, there is growing evidence that HO-1 plays an important role in anti-inflammatory, anti-apoptosis, pro-angiogenesis, and maintaining skeletal muscle homeostasis, making it a potential therapeutic target for improving skeletal muscle atrophy. Here, we review the pathogenesis of skeletal muscle atrophy, the biology of HO-1 and its regulation, and the biological function of HO-1 in skeletal muscle homeostasis, with a specific focus on the role of HO-1 in skeletal muscle atrophy, aiming to observe the therapeutic potential of HO-1 for skeletal muscle atrophy.

Regular exercise attenuates alcoholic myopathy in zebrafish by modulating mitochondrial homeostasis.

Alcoholic myopathy is caused by chronic consumption of alcohol (ethanol) and is characterized by weakness and atrophy of skeletal muscle. Regular exercise is one of the important ways to prevent or alleviate skeletal muscle myopathy. However, the beneficial effects and the exact mechanisms underlying regular exercise on alcohol myopathy remain unclear. In this study, a model of alcoholic myopathy was established using zebrafish soaked in 0.5% ethanol. Additionally, these zebrafish were intervened to swim for 8 weeks at an exercise intensity of 30% of the absolute critical swimming speed (Ucrit), aiming to explore the beneficial effects and underlying mechanisms of regular exercise on alcoholic myopathy. This study found that regular exercise inhibited protein degradation, improved locomotion ability, and increased muscle fiber cross-sectional area (CSA) in ethanol-treated zebrafish. In addition, regular exercise increases the functional activity of mitochondrial respiratory chain (MRC) complexes and upregulates the expression levels of MRC complexes. Regular exercise can also improve oxidative stress and mitochondrial dynamics in zebrafish skeletal muscle induced by ethanol. Additionally, regular exercise can activate mitochondrial biogenesis and inhibit mitochondrial unfolded protein response (UPRmt). Together, our results suggest regular exercise is an effective intervention strategy to improve mitochondrial homeostasis to attenuate alcoholic myopathy.

Patient-specific computational fluid dynamics for hypertrophic obstructive cardiomyopathy.

BACKGROUND: The heterogeneous morphologic and functional expression of hypertrophic obstructive cardiomyopathy (HOCM) is evidenced by established imaging, multimodality imaging is essential for a comprehensive assessment but may remain uncertain. This study aimed to develop a patient-specific hemodynamics assessment with cardiac computed tomography angiography (CCTA) based computational fluid dynamics (CFD) and prove its usability in cohorts of HOCM patients. METHODS: A retrospective study was performed on eight HOCM patients with septal myectomy who had both preoperative and postoperative CCTA as well as transthoracic echocardiography (TTE). The three-dimensional models were reconstructed from CCTA data, following which patient-specific CFD simulations were performed to estimate the blood velocity, pressure gradient, and wall shear stress. The simulation output was compared with TTE. Based on CFD simulations, retrospective and blinded virtual myectomy was also performed, to predict the minimum resected volume for improving obstruction in patients. RESULT: The complex HOCM anatomy was successfully reconstructed for all 8 patients. The CFD simulation accurately assessed the pressure gradient, flow velocity. There was a good correlation between the peak pressure gradient measured by CFD and TTE in the pre- and post-operative assessments (r = 0.87 and 0.84, respectively), and the flow velocity (r = 0.87 and 0.90, respectively). The volumes of minimal resection myocardium predicted by CFD and virtual myectomy were consistent with the actual resection volumes. CONCLUSION: CCTA-based CFD for HOCM patients may play a unique role in the assessment of patient-specific morphology and hemodynamics. Combination with virtual myectomy might allow for optimizing therapy planning in septal myectomy. CLINICAL PERSPECTIVE: CFD based CCTA may emerge as a complement to established imaging strategies, with accurate three-dimensional reconstruction and hemodynamic simulation of the left ventricle in this retrospective study. Combined with virtual myectomy, CFD simulation might allow for predicting the volume of resected myocardium for septal myectomy. Moving forward, this technology may be used by clinicians to better assess the conditions of HOCM patients, and guide the extent and depth of resection during septal myectomy. Therefore, further prospective clinical evaluation is clearly warranted.

Aerobic exercise enhances mitochondrial homeostasis to counteract D-galactose-induced sarcopenia in zebrafish.

Sarcopenia is a common skeletal muscle degenerative disease characterized by decreased skeletal muscle mass and mitochondrial dysfunction that involves microRNAs (miR) as regulatory factors in various pathways. Exercise reduces age-related oxidative damage and chronic inflammation and increases autophagy, among others. Moreover, whether aerobic exercise can regulate mitochondrial homeostasis by modulating the miR-128/insulin-like growth factor-1 (IGF-1) signaling pathway and can improve sarcopenia requires further investigation. Interestingly, zebrafish have been used as a model for aging research for over a decade due to their many outstanding advantages. Therefore, we established a model of zebrafish sarcopenia using d-galactose immersion and observed substantial changes, including reduced skeletal muscle cross-sectional area, increased tissue fibrosis, decreased motility, increased skeletal muscle reactive oxygen species, and notable alterations in mitochondrial morphology and function. We found that miR-128 expression was considerably upregulated, where as Igf1 and peroxisome proliferator-activated receptor gamma coactivator 1-alpha were significantly downregulated; moreover, mitochondrial homeostasis was reduced. Four weeks of aerobic exercise delayed sarcopenia progression and prevented the disruption of mitochondrial function and homeostasis. The genes related to atrophy and miR-128 were downregulated, Igf1 expression was considerably upregulated, and the phosphorylation levels of Pi3k, Akt, and Foxo3a were upregulated. Furthermore, mitochondrial respiration and homeostasis were enhanced. In conclusion, aerobic exercise improved skeletal muscle quality and function via the miR-128/IGF-1 signaling pathway, consequently ameliorating mitochondrial homeostasis in aging skeletal muscle.

Progress on the study of Popeye domain-containing 3 (POPDC3) in malignancies and striated muscle function and homeostasis.

The Popeye domain-containing protein 3 (POPDC3), a transmembrane protein with a unique cyclic adenosine monophosphate (cAMP) binding site, is widely expressed in mammalian tissues, with the highest levels of expression in skeletal muscle. POPDC3 plays a key role in many physiological and pathological processes and is considered a candidate biomarker and potential therapeutic target of cancer. In addition, POPDC3 gene variants have been associated with limb-girdle muscular dystrophy (LGMD) type 26. However, there are only a few studies on the biological role of POPDC3, interacting proteins, potential downstream targets, and regulated signaling pathways. Therefore, this review focuses on the structure of POPDC3 protein, interacting molecules, and the role and mechanism in cancer, and in cardiac and skeletal muscle, and to review the current research progress of POPDC3 and propose possible future study directions.

A rare combination of Ebstein's anomaly with left ventricular outflow tract obstruction.

We describe a rare case of Ebstein's anomaly (EA) combined with left ventricular outflow tract obstruction in a 54-year-old man that was accurately identified by echocardiography, cardiac magnetic resonance imaging (CMR). The imaging result was ultimately validated by surgery. We emphasize the clinical importance of using echocardiography and CMR together to provide a thorough, noninvasive explanation of these results.

Two-Color Cholesteric Liquid Crystalline Gels for Reversible Writing and Erasing Information Encryption.

Bright structural color derived from the unique helical superstructure of cholesteric liquid crystals (CLCs) has attracted much attention. In addition, fluorescence color is an intrinsic emission upon excitation, which can be observed often under UV light. However, it is a challenge to combine the fluorescence and structural colors to construct a self-supporting system at the same time. In this work, a photoresponsive cyanostilbene-based gelator (CSpy-C10) is synthesized, which emits blue fluorescence in LC. CSpy-C10 can gel LCs and further construct thermo-/photoresponsive CLC physical gels. The structural color of the CLCs, fluorescence, and mechanical properties of the gels can be independently regulated due to the separation of the chiral unit and photoresponsive unit with aggregation-induced emission behavior. Finally, the reversible information encryption including writing and erasing based on the changes in fluorescence are explored. This kind of two-color material can be applied in the fields ranging from information encryption, fluorescent display to high-tech anticounterfeiting.

Exercise intervention mitigates zebrafish age-related sarcopenia via alleviating mitochondrial dysfunction.

Sarcopenia is a common disorder that leads to a progressive decrease in skeletal muscle function in elderly people. Exercise effectively prevents or delays the onset and progression of sarcopenia. However, the molecular mechanisms underlying how exercise intervention improves skeletal muscle atrophy remain unclear. In this study, we found that 21-month-old zebrafish had a decreased swimming ability, reduced muscle fibre cross-sectional area, unbalanced protein synthesis, and degradation, increased oxidative stress, and mitochondrial dysfunction, which suggests zebrafish are a valuable model for sarcopenia. Eight weeks of exercise intervention attenuated these pathological changes in sarcopenia zebrafish. Moreover, the effects of exercise on mitochondrial dysfunction were associated with the activation of the AMPK/SIRT1/PGC-1α axis and 15-PGDH downregulation. Our results reveal potential therapeutic targets and indicators to treat age-related sarcopenia using exercise intervention.

Alcohol Induces Zebrafish Skeletal Muscle Atrophy through HMGB1/TLR4/NF-κB Signaling.

Excessive alcohol consumption can cause alcoholic myopathy, but the molecular mechanism is still unclear. In this study, zebrafish were exposed to 0.5% alcohol for eight weeks to investigate the effect of alcohol on skeletal muscle and its molecular mechanism. The results showed that the body length, body weight, cross-sectional area of the skeletal muscle fibers, Ucrit, and MO2max of the zebrafish were significantly decreased after alcohol exposure. The expression of markers of skeletal muscle atrophy and autophagy was increased, and the expression of P62 was significantly reduced. The content of ROS, the mRNA expression of sod1 and sod2, and the protein expression of Nox2 were significantly increased. In addition, we found that the inflammatory factors Il1ß and Tnfα were significantly enriched in skeletal muscle, and the expression of the HMGB1/TLR4/NF-κB signaling axis was also significantly increased. In summary, in this study, we established a zebrafish model of alcohol-induced skeletal muscle atrophy and further elucidated its pathogenesis.

Serial changes in left ventricular myocardial deformation in sepsis or septic shock using three-dimensional and two-dimensional speckle tracking echocardiography.

Background: This study aimed to investigate the serial changes in left ventricular (LV) myocardial deformation in patients with sepsis using three-dimensional (3D) and two-dimensional (2D) speckle tracking echocardiography (STE). Methods: In this single-center, prospective, and observational study, we included 59 patients diagnosed with sepsis or septic shock in the intensive care unit and 40 healthy controls. Left ventricular ejection fraction (LVEF), left ventricular global longitudinal strain (GLS), and global circumferential strain (GCS) assessed by 3D STE and 2D STE were obtained on the first, third, fifth, seventh to the tenth day after sepsis or septic shock. Results: In patients with sepsis or septic shock, 3D and 2D LVEF were not different at each time point. GLS and GCS obtained by 3D STE and 2D STE decreased on the first day compared with the healthy group (all P < 0.01). Compared with the values on the first day, GLS and GCS further decreased on the third day, while 3D and 2D LVEF did not differ. 3D and 2D STE strains were lowest on the third day and gradually improved on the seventh to the tenth day compared with values on the third day. When compared with values on the first day, 3D and 2D GLS gradually improved on the seventh to the tenth day, whereas 3D and 2D GCS on the seventh to the tenth day was not different. Although 3D and 2D STE strains were significantly increased on the seventh to the tenth day, they were not fully recovered to normality. Conclusion: Although patients with sepsis or septic shock demonstrated gradual improvements in 3D and 2D STE parameters during the ten-day period, LV myocardial strain was not fully recovered to normality by the seventh to the tenth days. 3D and 2D strain imaging, used as a helpful tool for monitoring the evolution of myocardial deformation, can provide clinicians with a useful additional imaging parameter.

Dry Heat as a Potential Decontamination Method on the Filtration Efficiency of Filtering Facepiece Respirators.

Filtering facepiece respirators have been widely used in the fields of occupational health and public hygiene, especially during the COVID-19 pandemic. In particular, disposable respirators have been in high demand, and the waste generated from these disposable products poses a problem for the environment. Here, we aimed to test a practical decontamination method to allow for the reuse of KN95 respirators. In this study, three types of KN95 respirators were heated at 80 °C and 90 °C for different durations (15 min, 30 min, 45 min, 1 h, 2 h, 3 h, 4 h, 6 h, 8 h, 10 h, and 24 h). The filtration efficiencies of the tested KN95 respirators before and after heating were measured, and the changes in microstructure were imaged with a scanning electron microscope (SEM). In addition, a neural network model based on the nonlinear autoregressive with external input (NARX) to predict the filtration efficiency of the KN95 respirator was established. The results show that the temperature and time of dry heating affected particle prevention. The higher the temperature and the longer the heating time, the more obvious the decline in the filtration efficiency of the respirators. When the heating temperature reached 100 °C, the respirator may be no longer suitable for reuse. These results show that a dry heat temperature between 70 °C and 90 °C, and a heating time between 30 min and 2 h is assumed to be a suitable and effective decontamination method for respirators.

Agonist-induced Piezo1 activation promote mitochondrial-dependent apoptosis in vascular smooth muscle cells.

OBJECTIVE: Mechanical damage plays an essential role in the progression of atherosclerosis. Piezo1 is a new mechanically sensitive ion channel. The present study investigated the vascular smooth muscle cells (VSMCs) apoptosis induced by Piezo1 activation and explored its underlying mechanism. METHODS: We evaluated cell viability and apoptosis rate with cell counting kit-8 (CCK-8) and Annexin V-FITC/PI flow cytometry assay, respectively. And then Western blot was performed to measure the relative protein. Reactive oxygen species (ROS) and intracellular Ca2+ were assessed via fluorescence microscope, and the mitochondrial transmembrane potential was monitored by JC-10 staining. RESULTS: Our in vitro study revealed that mice in the ApoE-/- group compared with control mice showed higher Piezo1 expression(P < 0.05). Besides, Yoda1, a Piezo1 agonist, triggered Ca2+ overload, mitochondrial damage, accumulation of ROS, and VSMCs apoptosis in a dose-depend manner. Furthermore, BAPT-AM (an intracellular Ca2+ chelator) and NAC (an antioxidant) suppressed the mitochondrial damage and attenuated the VSMCs apoptosis. CONCLUSION: Our study suggested that Piezo1 induced VSMCs apoptosis because of Ca2+ overload, excessive ROS generation, and mitochondrial dysfunction, which indicated that Piezo1 has potential value in treating vascular diseases.

A High-Fat Diet Induces Muscle Mitochondrial Dysfunction and Impairs Swimming Capacity in Zebrafish: A New Model of Sarcopenic Obesity.

Obesity is a highly prevalent disease that can induce metabolic syndrome and is associated with a greater risk of muscular atrophy. Mitochondria play central roles in regulating the physiological metabolism of skeletal muscle; however, whether a decreased mitochondrial function is associated with impaired muscle function is unclear. In this study, we evaluated the effects of a high-fat diet on muscle mitochondrial function in a zebrafish model of sarcopenic obesity (SOB). In SOB zebrafish, a significant decrease in exercise capacity and skeletal muscle fiber cross-sectional area was detected, accompanied by high expression of the atrophy-related markers Atrogin-1 and muscle RING-finger protein-1. Zebrafish with SOB exhibited inhibition of mitochondrial biogenesis and fatty acid oxidation as well as disruption of mitochondrial fusion and fission in atrophic muscle. Thus, our findings showed that muscle atrophy was associated with SOB-induced mitochondrial dysfunction. Overall, these results showed that the SOB zebrafish model established in this study may provide new insights into the development of therapeutic strategies to manage mitochondria-related muscular atrophy.

Helix Induction and Inversion of Polymeric Foldamer Regulated by the Single Enantiomers.

Generally, a single enantiomer can induce a foldamer into a preferred-handed helix, while another condition is required for the helical inversion. Herein, it is found that the helix induction and subsequent inversion of poly(m-phenylene diethynylene)-based foldamer bearing aza-18-crown-6 pendants (Poly-1) can be realized by increasing the concentration of sterically hindered l-amino acid perchlorate salts. When the amount of chiral enantiomers is small, one enantiomer tends to complex with two non-adjacent aza-18-crown-6 rings via three N+ H···O hydrogen bonds in a sandwich mode. Notably, the transition dipole moment is perpendicular to the aza-18-crown-6 ring, so that the induced helical chirality in Poly-1 backbone is opposite to the chirality of enantiomers. When the amount of chiral enantiomers is large enough, each aza-18-crown-6 is occupied by one enantiomer, which causes the transition dipole moment in a parallel direction to aza-18-crown-6 ring. In this case, the increased steric hindrance can facilitate the inversion of screw sense of Poly-1 backbone, which is directed by chiral center of enantiomers. As a result, a helix inversion has been achieved successfully. This work not only provides a novel strategy for regulating the two-stage folded helical conformations by the single enantiomers, but opens a window to develop chiral recognition materials.