Axial Higgs mode detected by quantum pathway interference in RTe3.

The observation of the Higgs boson solidified the standard model of particle physics. However, explanations of anomalies (for example, dark matter) rely on further symmetry breaking, calling for an undiscovered axial Higgs mode1. The Higgs mode was also seen in magnetic, superconducting and charge density wave (CDW) systems2,3. Uncovering the vector properties of a low-energy mode is challenging, and requires going beyond typical spectroscopic or scattering techniques. Here we discover an axial Higgs mode in the CDW system RTe3 using the interference of quantum pathways. In RTe3 (R = La, Gd), the electronic ordering couples bands of equal or different angular momenta4-6. As such, the Raman scattering tensor associated with the Higgs mode contains both symmetric and antisymmetric components, which are excited via two distinct but degenerate pathways. This leads to constructive or destructive interference of these pathways, depending on the choice of the incident and Raman-scattered light polarization. The qualitative behaviour of the Raman spectra is well captured by an appropriate tight-binding model, including an axial Higgs mode. Elucidation of the antisymmetric component is direct evidence that the Higgs mode contains an axial vector representation (that is, a pseudo-angular momentum) and hints that the CDW is unconventional. Thus, we provide a means for measuring quantum properties of collective modes without resorting to extreme experimental conditions.

Nucleosomal elements that control the topography of the barrier to transcription.

The nucleosome represents a mechanical barrier to transcription that operates as a general regulator of gene expression. We investigate how each nucleosomal component-the histone tails, the specific histone-DNA contacts, and the DNA sequence-contributes to the strength of the barrier. Removal of the tails favors progression of RNA polymerase II into the entry region of the nucleosome by locally increasing the wrapping-unwrapping rates of the DNA around histones. In contrast, point mutations that affect histone-DNA contacts at the dyad abolish the barrier to transcription in the central region by decreasing the local wrapping rate. Moreover, we show that the nucleosome amplifies sequence-dependent transcriptional pausing, an effect mediated through the structure of the nascent RNA. Each of these nucleosomal elements controls transcription elongation by affecting distinctly the density and duration of polymerase pauses, thus providing multiple and alternative mechanisms for control of gene expression by chromatin remodeling and transcription factors.

Factors influencing health-related quality of life in women with endometriosis: A cross-sectional study.

This study aimed to assess the health-related quality of life and identify its associated factors in women with endometriosis. A cross-sectional correlation study design and convenience sampling were conducted in the gynecological outpatient clinic of a teaching hospital in northern Taiwan. A total of 216 women with endometriosis were recruited. The data were collected using structured questionnaires and analyzed using descriptive and inferential statistics. Participants reported a moderate level of health-related quality of life. The most significant impact of endometriosis on health-related quality of life was emotional well-being, followed by feeling of control or powerless, pain, social support, and self-image. Educational attainment, menstrual cycle, period length, perceived menstrual flow, symptom distress, and self-management strategies explained 66% of the variance in health-related quality of life. Factors influencing health-related quality of life in women with endometriosis play a key role in promoting women's well-being. Interventions based on these related factors should be developed and taken into practice to effectively manage the disease-related symptoms for women with endometriosis and thereby improve their overall health-related quality of life.

The CLIP-170 N-terminal domain binds directly to both F-actin and microtubules in a mutually exclusive manner.

The cooperation between the actin and microtubule (MT) cytoskeletons is important for cellular processes such as cell migration and muscle cell development. However, a full understanding of how this cooperation occurs has yet to be sufficiently developed. The MT plus-end tracking protein CLIP-170 has been implicated in this actin-MT coordination by associating with the actin-binding signaling protein IQGAP1 and by promoting actin polymerization through binding with formins. Thus far, the interactions of CLIP-170 with actin were assumed to be indirect. Here, we demonstrate using high-speed cosedimentation assays that CLIP-170 can bind to filamentous actin (F-actin) directly. We found that the affinity of this binding is relatively weak but strong enough to be significant in the actin-rich cortex, where actin concentrations can be extremely high. Using CLIP-170 fragments and mutants, we show that the direct CLIP-170-F-actin interaction is independent of the FEED domain, the region that mediates formin-dependent actin polymerization, and that the CLIP-170 F-actin-binding region overlaps with the MT-binding region. Consistent with these observations, in vitro competition assays indicate that CLIP-170-F-actin and CLIP-170-MT interactions are mutually exclusive. Taken together, these observations lead us to speculate that direct CLIP-170-F-actin interactions may function to reduce the stability of MTs in actin-rich regions of the cell, as previously proposed for MT end-binding protein 1.

Emergence and Persistent Dominance of SARS-CoV-2 Omicron BA.2.3.7 Variant, Taiwan.

Since April 2022, waves of SARS-CoV-2 Omicron variant cases have surfaced in Taiwan and spread throughout the island. Using high-throughput sequencing of the SARS-CoV-2 genome, we analyzed 2,405 PCR-positive swab samples from 2,339 persons and identified the Omicron BA.2.3.7 variant as a major lineage within recent community outbreaks in Taiwan.

SUMO-Activating Enzyme Subunit 1 Is Associated with Poor Prognosis, Tumor Progression, and Radio-Resistance in Colorectal Cancer.

Concurrent chemoradiotherapy is an effective treatment option for patients with low-grade colorectal cancer (CRC) in the local disease stage. At present, the principle of the Taiwan Medical Center is to treat CRC patients with combination radiotherapy and chemotherapy (high-dose 5-FU) for a period of about five weeks prior to surgery. Radical resection of the tumor is performed at least six to eight weeks after concurrent chemoradiotherapy (CCRT). However, this approach fails to produce the desired therapeutic effect in approximately 20% to 30% of patients, and such patients are unnecessarily exposed to the risks of radiation and drug toxicity posed by this therapy. Therefore, it is crucial to explore new biomarkers to predict the prognosis of CRC. SUMO-activating enzyme subunit 1 (SAE1) plays an important role in SUMOylation, a post-translational modification involved in cellular functions, such as cell proliferation, cell cycle, and apoptosis. In our study, to explore the clinical-pathological role of SAE1 protein in CRC, we evaluated the clinical data and paraffin sections from CRC patients. The expression of SAE1 was evaluated using immunohistochemical analysis, and clinical parameters were analyzed using chi-square and Kaplan-Meier survival tests. The results of in vitro proliferation and radiosensitive assays were compared between control groups and SAE1 siRNA groups. Western blotting was also used to detect the expressions of the SAE1, PARP, cyclin D1, p-NF-κB, and NF-κB proteins. Flow cytometry and colony formation assays were used to detect the effect of SAE-1 on radiosensitivity. In vivo, we detected the growth curve in a mouse xenograft model. The results showed that SAE-1 was revealed to be an independent prognostic biomarker of CRC. SAE1 knockdown inhibited CRC proliferation in vitro and in vivo, and led to the cleavage of PARP, downregulation of cyclin D1 protein expression, and downregulation of p-NF-κB/NF-κB. Additionally, SAE1 knockdown promoted radiosensitivity in CRC cells. Therefore, it was inferred that SAE1 may be used as a potential therapeutic target in CRC treatment.

The cellular responses of corneal fibroblasts to cyclic stretching loads.

Mechanical signaling plays a crucial role in maintaining extracellular matrix (ECM) homeostasis in various structures. In this study, we investigated the responses of corneal fibroblasts to cyclic stretching loads using an in vitro cell culture system. Bovine corneal fibroblasts were cultured and subjected to equibiaxial cyclic strain of 15% for 72 h at a frequency of 0.25 Hz, with bovine skin fibroblasts used as a comparison. We explored various cellular behaviors, including morphological changes, cell proliferation, and metabolism in response to mechanical stretching loads. The expression of genes, protein secretion, and enzymatic activity for several major metalloproteinases was also determined through Q-PCR, Western blot, and gel zymography. Additionally, we investigated the involvement of mitogen-activated protein kinases (MAPKs) signaling pathways in the corneal fibroblasts when subjected to mechanical stimuli. Our findings revealed that, compared to skin fibroblasts, corneal fibroblasts were reluctant to morphological changes in response to a prolonged (72 h) and high-amplitude (15% of strain) cyclic stretching load. However, cyclic stretching loads stimulated the upregulation of MMP-2 expression in corneal fibroblasts via the MAPK signaling pathways involving extracellular signal-regulated kinase and p38. Together with a lack of upregulation in type I collagen expression, our results indicate the induction of the ECM degradation process in corneal fibroblasts in response to cyclic stretching. These findings emphasize the mechanoresponsive nature of corneal fibroblasts and shed light on the potential impact of intense mechanical stress on the cornea in both normal and pathological conditions such as keratoconus, providing valuable insights for understanding corneal mechanobiology.

Phenotypic heterogeneity in human genetic diseases: ultrasensitivity-mediated threshold effects as a unifying molecular mechanism.

Phenotypic heterogeneity is very common in genetic systems and in human diseases and has important consequences for disease diagnosis and treatment. In addition to the many genetic and non-genetic (e.g., epigenetic, environmental) factors reported to account for part of the heterogeneity, we stress the importance of stochastic fluctuation and regulatory network topology in contributing to phenotypic heterogeneity. We argue that a threshold effect is a unifying principle to explain the phenomenon; that ultrasensitivity is the molecular mechanism for this threshold effect; and discuss the three conditions for phenotypic heterogeneity to occur. We suggest that threshold effects occur not only at the cellular level, but also at the organ level. We stress the importance of context-dependence and its relationship to pleiotropy and edgetic mutations. Based on this model, we provide practical strategies to study human genetic diseases. By understanding the network mechanism for ultrasensitivity and identifying the critical factor, we may manipulate the weak spot to gently nudge the system from an ultrasensitive state to a stable non-disease state. Our analysis provides a new insight into the prevention and treatment of genetic diseases.

Observation of Ultrastrong Coupling between Substrate and the Magnetic Topological Insulator MnBi2Te4.

The intrinsic magnetic topological insulator MnBi2Te4 has attracted significant interest recently as a promising platform for exploring exotic quantum phenomena. Here we report that, when atomically thin MnBi2Te4 is deposited on a substrate such as silicon oxide or gold, there is a very strong mechanical coupling between the atomic layer and the supporting substrate. This is manifested as an intense low-frequency breathing Raman mode that is present even for monolayer MnBi2Te4. Interestingly, this coupling turns out to be stronger than the interlayer coupling between the MnBi2Te4 atomic layers. We further found that these low-energy breathing modes are highly sensitive to sample degradation, and they become drastically weaker upon ambient air exposure. This is in contrast to the higher energy optical phonon modes which are much more robust, suggesting that the low-energy Raman modes found here can be an effective indicator of sample quality.

Using Transfer Learning of Convolutional Neural Network on Neck Radiographs to Identify Acute Epiglottitis.

Acute epiglottitis (AE) is a life-threatening condition and needs to be recognized timely. Diagnosis of AE with a lateral neck radiograph yields poor reliability and sensitivity. Convolutional neural networks (CNN) are powerful tools to assist the analysis of medical images. This study aimed to develop an artificial intelligence model using CNN-based transfer learning to identify AE in lateral neck radiographs. All cases in this study are from two hospitals, a medical center, and a local teaching hospital in Taiwan. In this retrospective study, we collected 251 lateral neck radiographs of patients with AE and 936 individuals without AE. Neck radiographs obtained from patients without and with AE were used as the input for model transfer learning in a pre-trained CNN including Inception V3, Densenet201, Resnet101, VGG19, and Inception V2 to select the optimal model. We used five-fold cross-validation to estimate the performance of the selected model. The confusion matrix of the final model was analyzed. We found that Inception V3 yielded the best results as the optimal model among all pre-train models. Based on the average value of the fivefold cross-validation, the confusion metrics were obtained: accuracy = 0.92, precision = 0.94, recall = 0.90, and area under the curve (AUC) = 0.96. Using the Inception V3-based model can provide an excellent performance to identify AE based on radiographic images. We suggest using the CNN-based model which can offer a non-invasive, accurate, and fast diagnostic method for AE in the future.

Targeting ER protein TXNDC5 in hepatic stellate cell mitigates liver fibrosis by repressing non-canonical TGFß signalling.

BACKGROUND AND OBJECTIVES: Liver fibrosis (LF) occurs following chronic liver injuries. Currently, there is no effective therapy for LF. Recently, we identified thioredoxin domain containing 5 (TXNDC5), an ER protein disulfide isomerase (PDI), as a critical mediator of cardiac and lung fibrosis. We aimed to determine if TXNDC5 also contributes to LF and its potential as a therapeutic target for LF. DESIGN: Histological and transcriptome analyses on human cirrhotic livers were performed. Col1a1-GFPTg , Alb-Cre;Rosa26-tdTomato and Tie2-Cre/ERT2;Rosa26-tdTomato mice were used to determine the cell type(s) where TXNDC5 was induced following liver injury. In vitro investigations were conducted in human hepatic stellate cells (HSCs). Col1a2-Cre/ERT2;Txndc5fl/fl (Txndc5cKO ) and Alb-Cre;Txndc5fl/fl (Txndc5Hep-cKO ) mice were generated to delete TXNDC5 in HSCs and hepatocytes, respectively. Carbon tetrachloride treatment and bile duct ligation surgery were employed to induce liver injury/fibrosis in mice. The extent of LF was quantified using histological, imaging and biochemical analyses. RESULTS: TXNDC5 was upregulated markedly in human and mouse fibrotic livers, particularly in activated HSC at the fibrotic foci. TXNDC5 was induced by transforming growth factor ß1 (TGFß1) in HSCs and it was both required and sufficient for the activation, proliferation, survival and extracellular matrix production of HSC. Mechanistically, TGFß1 induces TXNDC5 expression through increased ER stress and ATF6-mediated transcriptional regulation. In addition, TXNDC5 promotes LF by redox-dependent JNK and signal transducer and activator of transcription 3 activation in HSCs through its PDI activity, activating HSCs and making them resistant to apoptosis. HSC-specific deletion of Txndc5 reverted established LF in mice. CONCLUSIONS: ER protein TXNDC5 promotes LF through redox-dependent HSC activation, proliferation and excessive extracellular matrix production. Targeting TXNDC5, therefore, could be a potential novel therapeutic strategy to ameliorate LF.

Depilatory laser miniaturizes hair by inducing bystander dermal papilla cell necrosis through thermal diffusion.

OBJECTIVES: Depilatory laser targeting melanin has been widely applied for the treatment of hypertrichosis. Both selective photothermolysis and thermal diffusion have been proposed for its effect, but the exact mechanism of permanent hair reduction remains unclear. In this study, we explore the role of thermal diffusion in depilatory laser-induced permanent hair loss and determine whether nonpigmented cells are injured by thermal diffusion. MATERIALS AND METHODS: C57BL/6 mice in anagen and telogen were treated with alexandrite laser (wavelength 755 nm, pulse duration 3 milliseconds, fluence 12 J/cm2 , spot size 12 mm), respectively. Histological analysis, terminal deoxynucleotidyl transferase dUTP nick-end labeling assay, and transmission electron microscopic imaging were employed to evaluate the injury to hair follicle (HF) cells. The proliferation status of HF cells was examined by 5-bromo-2'-deoxyuridine pulse labeling. The number of HF stem cells was quantified by fluorescence-activated cell sorting. The size of the regenerated hair was determined by measuring its length and width. RESULTS: We found that irradiating C57BL/6 mice in anagen with alexandrite laser led to hair miniaturization in the next anagen. In addition to thermal disruption of melanin-containing cells in the precortex region, we also detected necrosis of the adjacent nonpigmented dermal papilla cells due to thermal diffusion. Dermal papilla cells decreased by 24% after laser injury, while the number of bulge stem cells remained unchanged. When the laser was delivered to telogen HFs where no melanin was present adjacent to the dermal papilla, thermal necrosis and cell reduction were not detected in the dermal papilla and no hair miniaturization was observed. CONCLUSION: Our results suggest that depilatory laser miniaturizes hair by inducing thermal necrosis of dermal papilla cells due to secondary thermal diffusion from melanin-containing precortex cells in the anagen hair bulbs.

Emergent Roles of Circular RNAs in Metabolism and Metabolic Disorders.

Circular RNAs (circRNAs) are an emerging group of long non-coding RNAs (lncRNAs) and have attracted attention again according to the progress in high-throughput sequencing in recent years. circRNAs are genome transcripts produced from pre-messenger (m)RNA regions in a specific process called "back-splicing," which forms covalently closed continuous loops. Due to their lack of a 5' cap and 3' poly-adenylated tails, circRNAs are remarkably more stable than linear RNAs. Functionally, circRNAs can endogenously sponge to microRNAs, interact with RNA-binding proteins (RBPs), or translate themselves. Moreover, circRNAs can be expressed in cell type- or tissue-specific expression patterns. Therefore, they are proposed to play essential roles in fine-tuning our body's homeostasis by regulating transcription and translation processes. Indeed, there has been accumulating emergent evidence showing that dysregulation of circRNAs can lead to metabolic disorders. This study explored the current knowledge of circRNAs that regulate molecular processes associated with glucose and lipid homeostasis and related pathogeneses of metabolic disorders. We also suggest the potential role of circRNAs as disease biomarkers and therapeutic targets.

Increased Climbing Fiber Lateral Crossings on Purkinje Cell Dendrites in the Cerebellar Hemisphere in Essential Tremor.

BACKGROUND: Climbing fibers (CFs) innervate Purkinje cells (PCs) with 1:1 relationship to ensure proper cerebellar function. Although CFs abnormally extend into the parallel fiber domain of PC dendrites in essential tremor (ET), the architecture of CFs in relation to PCs has yet to be investigated in detail. OBJECTIVE: The aim of this work was to study the architecture of CFs in relation to PCs in ET. METHODS: The number of PC somas and PC dendrites that a single CF crossed was quantified in the postmortem cerebellum of 15 ET cases and 15 control cases. RESULTS: In ET, CFs crossed a greater number of PC somas and PC dendrites than in control cases, raising the possibility that there is abnormal CF wiring onto the PCs. Interestingly, the increase in CF-PC crossings positively correlated with tremor severity. CONCLUSIONS: Patients with ET have increased CF crossings on PC dendrites. This abnormal architectural arrangement may contribute to synchronous brain activity and tremor. © 2021 International Parkinson and Movement Disorder Society.

Negative valley polarization in doped monolayer MoSe2.

Monolayer molybdenum di-selenide (1L-MoSe2) stands out in the transition metal dichalcogenide family of materials as an outlier where optical generation of valley polarization is inefficient. Here we show that using charge doping in conjunction with an external magnetic field, the valley polarization of 1L-MoSe2 can be controlled effectively. Most remarkably, the valley polarization can be tuned to negative values, where the higher energy Zeeman mode emission is more intense than the lower energy one. Our experimental observations are interpreted with valley-selective exciton-charge dressing that manifests when gate induced doping populates predominantly one valley in the presence of Zeeman splitting.

Inhibition of miR-155 potentially protects against lipopolysaccharide-induced acute lung injury through the IRF2BP2-NFAT1 pathway.

Sepsis-induced lung injury is a lethal complication with no effective treatment options, affecting millions of people worldwide. Oroxylin A (OroA) is a natural flavonoid with potent anticancer effects, but its modulating effect on inflammation through microRNAs (miRs) is not apparent. In this report, we investigated the target genes of the miR pathway mediated by OroA and assessed the potential for novel treatments of septic lung injury. An miR array screening and quantitative polymerase chain reaction identified that miR-155-5p could be a candidate regulated by OroA. Bioinformatics analysis indicated that interferon regulatory factor-2-binding protein-2 (IRF2BP2) might be a target of miR-155-5p, and this hypothesis was verified through reporter assays. In addition, an immunoprecipitation assay demonstrated that OroA increased the binding activity of IRF2BP2 to the nuclear factor of activated T-cells 1 (NFAT1), causing inducible nitric oxide synthase to cause an inflammatory reaction. Finally, the direct injection of short hairpin RNA (shRNA)-miR-155-5p into the bone marrow of mice ameliorated LPS-induced acute lung injury and inflammation in mice. Our results provide new mechanistic insights into the role of the OroA-induced miR-155-5p-IRF2BP2-NFAT1 axis in sepsis, demonstrating that direct bone marrow injection of lentivirus containing shRNA-155-5p could prove to be a potential future clinical application in alleviating sepsis-induced acute lung injury.

Hinokitiol reduces tumor metastasis by inhibiting heparanase via extracellular signal-regulated kinase and protein kinase B pathway.

Heparanase cleaves the extracellular matrix by degrading heparan sulfate that ultimately leads to cell invasion and metastasis; a condition that causes high mortality among cancer patients. Many of the anticancer drugs available today are natural products of plant origin, such as hinokitiol. In the previous report, it was revealed that hinokitiol plays an essential role in anti-inflammatory and anti-oxidation processes and promote apoptosis or autophagy resulting to the inhibition of tumor growth and differentiation. Therefore, this study explored the effects of hinokitiol on the cancer-promoting pathway in mouse melanoma (B16F10) and breast (4T1) cancer cells, with emphasis on heparanase expression. We detected whether hinokitiol can elicit anti-metastatic effects on cancer cells via wound healing and Transwell assays. Besides, mice experiment was conducted to observe the impact of hinokitiol in vivo. Our results show that hinokitiol can inhibit the expression of heparanase by reducing the phosphorylation of protein kinase B (Akt) and extracellular regulated protein kinase (ERK). Furthermore, in vitro cell migration assay showed that heparanase downregulation by hinokitiol led to a decrease in metastatic activity which is consistent with the findings in the in vivo experiment.

Ground and excited state exciton polarons in monolayer MoSe2.

Monolayer transition metal dichalcogenide semiconductors, with versatile experimentally accessible exciton species, offer an interesting platform for investigating the interaction between excitons and a Fermi sea of charges. Using hexagonal boron nitride encapsulated monolayer MoSe2, we study the impact of charge density tuning on the A and B series of exciton Rydberg states, including A:1s, A:2s, B:1s, and B:2s. The doping dependence of the A:2s state provides an opportunity to examine such interactions with greatly reduced exciton binding energy and more spatially diffuse structures, and we found that the impact of the Fermi sea becomes much more dramatic compared to the A:1s state. Using photoluminescence upconversion, we verify that the B:2s exciton state displays similar behavior when interacting with the Fermi sea despite being well above the bare bandgap in energy. Photoluminescence and reflection spectra of the A:1s state show clear evidence that the interaction of the exciton with a Fermi sea is best described by the exciton-polaron model, rather than a trion model. Our experimental results demonstrate that overall features of charge interaction are quite generic and highly robust, offering key insights into the dressed many body states in a Fermi sea.

Online Survey of Digital Reading by Adults with Low Vision.

SIGNIFICANCE: Access to digital text is increasingly widespread, but its impact on low-vision reading is not well understood. PURPOSE: We conducted an online survey of people with low vision to determine what assistive technologies they use for visual reading, their preferred text characteristics, and the time they devote to reading digital and hard-copy text. METHODS: One hundred thirty-three low-vision participants completed an online survey. Participants reported the nature and history of their low vision, their usage of different assistive technologies, and time devoted to five visual reading activities. RESULTS: The three largest diagnostic categories were albinism (n = 36), retinitis pigmentosa (n = 20), and glaucoma (n = 15). Mean self-reported acuity was 0.93 logMAR (range, 0.1 to 1.6 logMAR). Mean age was 46 years (range, 18 to 98 years). Participants reported on percentage time spent reading using vision, audio, or touch (braille). Seventy-five percent of our participants did more than 50% of their reading visually. Across five categories of reading activities-work or education, news, pleasure, spot reading, and social networking-participants reported more time spent on digital reading than hard-copy reading. Eighty-nine percent of our participants used at least one technology from each of our two major categories of assistive technologies (digital content magnifiers and hard-copy content magnifiers) for visual reading. CONCLUSIONS: Despite the growing availability of digital text in audio or braille formats, our findings from an online sample of people with low vision indicate the continuing importance of visual reading. Our participants continue to use technology to access both hard-copy and digital text, but more time is devoted to digital reading. Our findings highlight the need for continued research and development of technology to enhance visual reading accessibility.

MicroRNAs as Biomarkers and Therapeutic Targets in Inflammation- and Ischemia-Reperfusion-Related Acute Renal Injury.

Acute kidney injury (AKI), caused mainly by ischemia-reperfusion, sepsis, or nephrotoxins (such as contrast medium), is identified by an abrupt decline in kidney function and is associated with high morbidity and mortality. Despite decades of efforts, the pathogenesis of AKI remains poorly understood, and effective therapies are lacking. MicroRNAs (miRNAs) are small noncoding RNAs that regulate gene expression at the posttranscriptional level to control cell differentiation, development, and homeostasis. Additionally, extracellular miRNAs might mediate cell-cell communication during various physiological and pathological processes. Recently, mounting evidence indicates that miRNAs play a role in the pathogenesis of AKI. Moreover, emerging research suggests that because of their remarkable stability in body fluids, microRNAs can potentially serve as novel diagnostic biomarkers of AKI. Of note, our previous finding that miR-494 is rapidly elevated in urine but not in serum provides insight into the ultimate role of urine miRNAs in AKI. Additionally, exosomal miRNAs derived from stem cells, known as the stem cell secretome, might be a potential innovative therapeutic strategy for AKI. This review aims to provide new data obtained in this field of research. It is hoped that new studies on this topic will not only generate new insights into the pathophysiology of urine miRNAs in AKI but also might lead to the precise management of this fatal disease.