MiR-1307-5p enhances fibroblast transdifferentiation to exacerbate chronic obstructive pulmonary disease through regulating FBXL16/HIF1α axis.

Chronic obstructive pulmonary disease (COPD) is an irreversible and progressive chronic inflammatory lung disease which affects millions of people worldwide. Activated fibroblasts are observed to accumulate in lung of COPD patients and promote COPD progression through aberrant extracellular matrix (ECM) deposition. In this study, we identified that miR-1307-5p expression was significantly increased in lung fibroblasts derived from COPD patients. Mechanistically, we found that upregulation of miR-1307-5p promoted TGF-ß induced lung fibroblast activation and transdifferentiation. We also identified FBXL16 as a direct target for miR-1307-5p mediated myofibroblast activation in COPD. Knockdown of FBXL16 by siRNA prominently increased the expression of myofibroblast markers in MRC-5 fibroblasts after TGF-ß administration. Ectopic expression of FBXL16 in MRC-5 counteracted miR-1307-5p agomir-induced fibroblast transdifferentiation. Furthermore, We found that miR-1307-5p promoted pulmonary fibroblast transdifferentiation through FBXL16 regulated HIF1α degradation. In general, our findings indicate that miR-1307-5p is important for COPD pathogenesis, and may serve as a potential target for COPD treatment.

A portent of catastrophic carbon dioxide embolism in laparoscopic hepatectomy: A case report.

INTRODUCTION: Laparoscopic hepatectomy (LH) poses a high risk of carbon dioxide embolism due to extensive hepatic transection, long surgery duration, and dissection of the large hepatic veins or vena cava. PATIENT CONCERNS: A 65-year-old man was scheduled to undergo LH. Following intraperitoneal carbon dioxide (CO2) insufflation and hepatic portal occlusion, the patient developed severe hemodynamic collapse accompanied by a decrease in the pulse oxygen saturation (SpO2). DIAGNOSIS: Although a decrease in end-tidal carbon dioxide (ETCO2) was not observed, CO2 embolism was still suspected because of the symptoms. INTERVENTIONS AND OUTCOMES: The patient was successfully resuscitated after the immediate discontinuation of CO2 insufflation and inotrope administration. CO2 embolism must always be suspected during laparoscopic surgery whenever sudden hemodynamic collapse associated with decreased pulse oxygen saturation occurs, regardless of whether ETCO2 changes. Instant arterial blood gas analysis is imperative, and a significant difference between PaCO2 and ETCO2 is indicative of carbon dioxide embolism. CONCLUSION: Instant arterial blood gas analysis is imperative, and a significant difference between PaCO2 and ETCO2 is indicative of carbon dioxide embolism.

MicroRNA-377-3p exacerbates chronic obstructive pulmonary disease through suppressing ZFP36L1 expression and inducing lung fibroblast senescence.

Chronic obstructive pulmonary disease (COPD) is a leading aging related cause of global mortality. Small airway narrowing is recognized as an early and significant factor for COPD development. Senescent fibroblasts were observed to accumulate in lung of COPD patients and promote COPD progression through aberrant extracellular matrix (ECM) deposition and senescence-associated secretory phenotype (SASP). On the basis of our previous study, we further investigated the the causes for the increased levels of miR-377-3p in the blood of COPD patients, as well as its regulatory function in the pathological progression of COPD. We found that the majority of up-regulated miR-377-3p was localized in lung fibroblasts. Inhibition of miR-377-3p improved chronic smoking-induced COPD in mice. Mechanistically, miR-377-3p promoted senescence of lung fibroblasts, while knockdown of miR-377-3p attenuated bleomycin-induced senescence in lung fibroblasts. We also identified ZFP36L1 as a direct target for miR-377-3p that likely mediated its pro senescence activity in lung fibroblasts. Our data reveal that miR-377-3p is crucial for COPD pathogenesis, and may serve as a potential target for COPD therapy.

Inhibition of TAF1B impairs ribosome biosynthesis and suppresses cell proliferation in stomach adenocarcinoma through promoting c-MYC mRNA degradation.

Hyperactivation of ribosome biosynthesis (RiBi) is a hallmark of cancer, and targeting ribosome biogenesis has emerged as a potential therapeutic strategy. The depletion of TAF1B, a major component of selectivity factor 1 (SL1), disrupts the pre-initiation complex, preventing RNA polymerase I from binding ribosomal DNA and inhibiting the hyperactivation of RiBi. Here, we investigate the role of TAF1B, in regulating RiBi and proliferation in stomach adenocarcinoma (STAD). We disclosed that the overexpression of TAF1B correlates with poor prognosis in STAD, and found that knocking down TAF1B effectively inhibits STAD cell proliferation and survival in vitro and in vivo. TAF1B knockdown may also induce nucleolar stress, and promote c-MYC degradation in STAD cells. Furthermore, we demonstrate that TAF1B depletion impairs rRNA gene transcription and processing, leading to reduced ribosome biogenesis. Collectively, our findings suggest that TAF1B may serve as a potential therapeutic target for STAD and highlight the importance of RiBi in cancer progression.

Major complications of caudal block: A prospective survey of 973 cases in adult anorectal surgery.

Background: We conducted a prospective study of surgical inpatients at a teaching hospital to assess the incidence and potential risk factors for major complications of caudal anesthesia in anorectal surgery. Methods: A total of 973 patients undergoing anorectal surgery under caudal block were included in this prospective, observer-blinded trial after providing consent. Demographic information, detailed perioperative information, anesthesia-related complications and postoperative follow-up information were recorded. Meanwhile, the incidence and risk factors for major caudal anesthesia-related complications were analyzed. Results: A total of 973 patients underwent caudal block. The effective rate was 95.38 % (928 cases). However, there were still 38 (3.91 %) cases with insufficient block and 7 (0.72 %) cases with no block. The major anesthesia-related complications were local anesthetic systemic toxicity (9, 0.92 %), cauda equine syndrome (1, 0.10 %), transient neurological symptoms (3, 0.31 %) and localized pain at the caudal insertion site (30, 3.08 %). The identified risk factor for local anesthetic systemic toxicity was multiple attempts locating the caudal space (OR = 5.30; 1.21-23.29). The identified risk factor for localized pain at the caudal insertion site was multiple attempts locating the caudal space (OR = 10.57; 4.89-22.86). Conclusion: The main complications of caudal block in adult patients are transient neurological symptoms, cauda equine syndrome, serious local anesthetic systemic toxicity and localized pain at the caudal insertion site. Overall, the incidence of complications is low and symptoms are mild. Caudal block is still a safe and reliable method for anesthesia in adult anorectal surgery.

Persistent postoperative hypotension caused by subclinical empty sella syndrome after a simple surgery: A case report.

BACKGROUND: Empty sella is an anatomical and radiological finding of the herniation of the subarachnoid space into the pituitary fossa leading to a flattened pituitary gland. Patients with empty sella may present with various symptoms, including headache due to intracranial hypertension and endocrine symptoms related to the specific pituitary hormones affected. Here, we report a female patient who developed persistent postoperative hypotension caused by subclinical empty sella syndrome after a simple surgery. CASE SUMMARY: A 47-year-old woman underwent vocal cord polypectomy under general anesthesia with endotracheal intubation. She denied any medical history, and her vital signs were normal before the surgery. Anesthesia and surgery were uneventful. However, she developed dizziness, headache and persistent hypotension in the ward. Thus, intravenous dopamine was started to maintain normal blood pressure, which improved her symptoms. However, she remained dependent on dopamine for over 24 h without any obvious anesthesia- and surgery-related complications. An endocrine etiology was then suspected, and further examination showed a high prolactin level, a low normal adrenocorticotropic hormone level and a low cortisol level. Magnetic resonance imaging of the brain revealed an empty sella. Therefore, she was diagnosed with empty sella syndrome and secondary adrenal insufficiency. Her symptoms disappeared one week later after daily glucocorticoid supplement. CONCLUSION: Endocrine etiologies such as pituitary and adrenal-related dysfunction should be considered in patients showing persistent postoperative hypotension when anesthesia- and surgery-related factors are excluded.

Development and validation of a nomogram for postoperative sleep disturbance in adults: a prospective survey of 640 patients undergoing spinal surgery.

BACKGROUND: Postoperative sleep disturbance (PSD) is a prevalent clinical complication that may arise due to various factors. The purpose of this investigation is to identify the risk factors for PSD in spinal surgery and establish a risk prediction nomogram. METHODS: The clinical records of individuals who underwent spinal surgery from January 2020 to January 2021 were gathered prospectively. The least absolute shrinkage and selection operator (LASSO) regression, along with multivariate logistic regression analysis, was employed to establish independent risk factors. A nomogram prediction model was devised based on these factors. The nomogram's effectiveness was evaluated and verified via the receiver operating characteristic (ROC) curve, calibration plot, and decision curve analysis (DCA). RESULTS: A total of 640 patients who underwent spinal surgery were analyzed in this investigation, among which 393 patients experienced PSD with an incidence rate of 61.4%. After conducting LASSO regression and logistic regression analyses using R software on the variables in training set, 8 independent risk factors associated to PSD were identified, including female, preoperative sleep disorder, high preoperative anxiety score, high intraoperative bleeding volume, high postoperative pain score, dissatisfaction with ward sleep environment, non-use of dexmedetomidine and non-use of erector spinae plane block (ESPB). The nomogram and online dynamic nomogram were constructed after incorporating these variables. In the training and validation sets, the area under the curve (AUC) in the receiver operating characteristic (ROC) curves were 0.806 (0.768-0.844) and 0.755 (0.667-0.844), respectively. The calibration plots indicated that the mean absolute error (MAE) values in both sets were respectively 1.2% and 1.7%. The decision curve analysis demonstrated the model had a substantial net benefit within the range of threshold probabilities between 20% and 90%. CONCLUSIONS: The nomogram model proposed in this study included eight frequently observed clinical factors and exhibited favorable accuracy and calibration. TRIAL REGISTRATION: The study was retrospectively registered with the Chinese Clinical Trial Registry (ChiCTR2200061257, 18/06/2022).

MicroRNA-155-5p inhibition alleviates irritable bowel syndrome by increasing claudin-1 and ZO-1 expression.

Background: Irritable bowel syndrome (IBS) is a common gastrointestinal disease. Emerging studies have demonstrated that microRNAs (miRNAs) are commonly dysregulated in patients with IBS, and aberrant miRNAs are implicated in IBS occurrence. Although miR-155-5p participates in inflammatory bowel disease (IBD) and intestinal barrier dysfunction, the role of miR-155-5p in IBS is unclear. Methods: In the present study, colon samples were obtained from IBS patients and IBS mice induced by trinitrobenzenesulfonic acid (TNBS), and the levels of miR-155-5p, claudin-1 (CLDN1), and zonula occludens-1 (ZO-1) were assessed using quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemical analysis. The regulatory role of miR-155-5p in CLDN1 and ZO-1 expression was validated using dual luciferase reporter assay. Results: We found that miR-155-5p levels were upregulated in colon samples of IBS patients and mice compared with healthy subjects and normal mice, respectively. Meanwhile, the levels of CLDN1 and ZO-1 were decreased in colon samples of IBS patients and mice. Importantly, forced expression of miR-155-5p inhibited CLDN1 and ZO-1 expression. In IBS mice, intraperitoneal injection with miR-155-5p inhibitor increased CLDN1 and ZO-1 expression in intestinal mucosal epithelium, enhanced visceral response thresholds, and decreased myeloperoxidase (MPO) activity. Conclusions: In summary, these results suggested that miR-155-5p participated in the pathogenesis of IBS, at least in part by inhibiting CLDN1 and ZO-1 expression, indicating that miR-155-5p may be a potential therapeutic target for IBS.

Highly synchronized cortical circuit dynamics mediate spontaneous pain in mice.

Cortical neural dynamics mediate information processing for the cerebral cortex, which is implicated in fundamental biological processes such as vision and olfaction, in addition to neurological and psychiatric diseases. Spontaneous pain is a key feature of human neuropathic pain. Whether spontaneous pain pushes the cortical network into an aberrant state and, if so, whether it can be brought back to a "normal" operating range to ameliorate pain are unknown. Using a clinically relevant mouse model of neuropathic pain with spontaneous pain-like behavior, we report that orofacial spontaneous pain activated a specific area within the primary somatosensory cortex (S1), displaying synchronized neural dynamics revealed by intravital two-photon calcium imaging. This synchronization was underpinned by local GABAergic interneuron hypoactivity. Pain-induced cortical synchronization could be attenuated by manipulating local S1 networks or clinically effective pain therapies. Specifically, both chemogenetic inhibition of pain-related c-Fos-expressing neurons and selective activation of GABAergic interneurons significantly attenuated S1 synchronization. Clinically effective pain therapies including carbamazepine and nerve root decompression could also dampen S1 synchronization. More important, restoring a "normal" range of neural dynamics through attenuation of pain-induced S1 synchronization alleviated pain-like behavior. These results suggest that spontaneous pain pushed the S1 regional network into a synchronized state, whereas reversal of this synchronization alleviated pain.

Research progress on the role of hormones in ischemic stroke.

Ischemic stroke is a major cause of death and disability around the world. However, ischemic stroke treatment is currently limited, with a narrow therapeutic window and unsatisfactory post-treatment outcomes. Therefore, it is critical to investigate the pathophysiological mechanisms following ischemic stroke brain injury. Changes in the immunometabolism and endocrine system after ischemic stroke are important in understanding the pathophysiological mechanisms of cerebral ischemic injury. Hormones are biologically active substances produced by endocrine glands or endocrine cells that play an important role in the organism's growth, development, metabolism, reproduction, and aging. Hormone research in ischemic stroke has made very promising progress. Hormone levels fluctuate during an ischemic stroke. Hormones regulate neuronal plasticity, promote neurotrophic factor formation, reduce cell death, apoptosis, inflammation, excitotoxicity, oxidative and nitrative stress, and brain edema in ischemic stroke. In recent years, many studies have been done on the role of thyroid hormone, growth hormone, testosterone, prolactin, oxytocin, glucocorticoid, parathyroid hormone, and dopamine in ischemic stroke, but comprehensive reviews are scarce. This review focuses on the role of hormones in the pathophysiology of ischemic stroke and discusses the mechanisms involved, intending to provide a reference value for ischemic stroke treatment and prevention.

Electroacupuncture attenuates surgical pain-induced delirium-like behavior in mice via remodeling gut microbiota and dendritic spine.

Surgical pain is associated with delirium in patients, and acupuncture can treat pain. However, whether electroacupuncture can attenuate the surgical pain-associated delirium via the gut-brain axis remains unknown. Leveraging a mouse model of foot incision-induced surgical pain and delirium-like behavior, we found that electroacupuncture stimulation at specific acupoints (e.g., DU20+KI1) attenuated both surgical pain and delirium-like behavior in mice. Mechanistically, mice with incision-induced surgical pain and delirium-like behavior showed gut microbiota imbalance, microglia activation in the spinal cord, somatosensory cortex, and hippocampus, as well as an enhanced dendritic spine elimination in cortex revealed by two-photon imaging. The electroacupuncture regimen that alleviated surgical pain and delirium-like behavior in mice also effectively restored the gut microbiota balance, prevented the microglia activation, and reversed the dendritic spine elimination. These data demonstrated a potentially important gut-brain interactive mechanism underlying the surgical pain-induced delirium in mice. Pending further studies, these findings revealed a possible therapeutic approach in preventing and/or treating postoperative delirium by using perioperative electroacupuncture stimulation in patients.

Prediction Model for Urinary Tract Infection in Pediatric Urological Surgery Patients.

Background: Urinary tract infection (UTI) is a common complication in pediatric urological surgery patients and is associated with long-term sequelae, including subsequent recurrent infections and renal scarring. In this study, we aimed to explore the risk factors for UTI in pediatric urological surgery patients and construct a predictive model for UTI. Materials and Methods: A total of 2,235 pediatric patients who underwent urological surgery at a tertiary hospital between February 2019 and January 2020 were included. A multivariate logistic regression model was applied to identify the predictive factors, and a predictive model was constructed using a receiver operating characteristic curve. A multifactorial predictive model was used to categorize the risk of UTI based on the weight of the evidence. Results: A total of 341 patients with UTI were identified, which corresponded to a prevalence of 15.26% in pediatric urological surgery patients. Multivariate analysis identified six significant risk factors for UTI, including age <12.0 months, upper urinary tract disease, not using an indwelling drainage tube, hospital stay ≥10 days, administration of two or more types of antibiotics, and stent implantation. A combination of the aforementioned factors produced an area under the curve value of 88.37% for preventing UTI in pediatric urological surgery patients. A multifactorial predictive model was created based on the combination of these factors. Conclusions: The constructed multifactorial model could predict UTI risk in pediatric urological surgery patients with a relatively high predictive value.

Recent Advances in Progresses and Prospects of IL-37 in Central Nervous System Diseases.

Interleukin-37 (IL-37) is an effective anti-inflammatory factor and acts through intracellular and extracellular pathways, inhibiting the effects of other inflammatory cytokines, such as IL-1ß, IL-6, and tumor necrosis factor-α (TNF-α), thereby exerting powerful anti-inflammatory effects. In numerous recent studies, the anti-inflammatory effects of IL-37 have been described in many autoimmune diseases, colitis, and tumors. However, the current research on IL-37 in the field of the central nervous system (CNS) is not only less, but mainly for clinical research and little discussion of the mechanism. In this review, the role of IL-37 and its associated inflammatory factors in common CNS diseases are summarized, and their therapeutic potential in CNS diseases identified.

Non-Linear Association between Folate/Vitamin B12 Status and Cognitive Function in Older Adults.

Although folate and vitamin B12 status have long been implicated in cognitive function, there is no consensus on the threshold of folate and vitamin B12 for assessing their impacts on cognition. The goal of this study was to detail the association between folate and vitamin B12 with cognitive performance. We analyzed cross-sectional data of older adults (≥60 y; n = 2204) from the NHANES (National Health and Nutrition Examination Surveys) cohort from 2011-2014. The restricted cubic spline model was used for describing the associations between serum total folate, RBC folate, 5-methyltetrahydrofolate, and vitamin B12 and the Consortium to Establish a Registry for Alzheimer's Disease Word Learning (CERAD-WL) and Delayed Recall (CERAD-DR) tests, the Animal Fluency (AF) test, and the Digit Symbol Substitution Test (DSST), respectively. Older adults with a different folate and vitamin B12 status were clustered by artificial intelligence unsupervised learning. The statistically significant non-linear relationships between the markers of folate or vitamin B12 status and cognitive function were found after adjustments for potential confounders. Inverse U-shaped associations between folate/vitamin B12 status and cognitive function were observed, and the estimated breakpoint was described. No statistically significant interaction between vitamin B12 and folate status on cognitive function was observed in the current models. In addition, based on the biochemical examination of these four markers, older adults could be assigned into three clusters representing relatively low, medium, and high folate/vitamin B12 status with significantly different scores on the CERAD-DR and DSST. Low or high folate and vitamin B12 status affected selective domains of cognition, and was associated with suboptimal cognitive test outcomes.

The protective effects of HIF-1α activation on sepsis induced intestinal mucosal barrier injury in rats model of sepsis.

The integrity of the intestinal barrier is critical for protecting the host against the pathogen. The role of hypoxia-inducible factor-1α (HIF-1α) in the intestinal barrier disfunction related to sepsis remained unclear. The purpose of the present study is to investigate the role of HIF-1α on oxidative damage, the intestinal mucosal permeability, structural and morphological changes during sepsis. Twenty-four Sprague Dawley (SD) rats were randomly divided into four groups of 6 rats each: the sham group (sham), sepsis group (subjected to cecal ligation and perforation, CLP), sepsis + DMOG group (40 mg/kg of DMOG by intraperitoneal injection for 7 consecutive days before CLP), and sepsis + BAY 87-2243 group (9 mg/kg of BAY 87-2243 orally administered for 3 consecutive days before CLP). Sepsis increased plasma levels of inflammatory mediators, oxidative stress markers and HIF-1α expression; caused pathological damage; increased permeability (P < 0.05); and decreased TJ protein expression in the intestinal mucosa of rats with sepsis (P < 0.05). The addition of DMOG up-regulated HIF-1α, then decreased the plasma levels of inflammatory mediators, oxidative stress markers, alleviated pathological damage to the intestinal mucosa and decreased intestinal permeability (P < 0.05); while BAY 87-2243 treatment had the opposite effects. Our findings showed that HIF-1α protects the intestinal barrier function of septic rats by inhibiting intestinal inflammation and oxidative damage, our results provide a novel insight for developing sepsis treatment.

Role of lipocalin-2 in surgery-induced cognitive decline in mice: a signal from neuron to microglia.

BACKGROUND: Perioperative neurocognitive disorders (PNDs) are common complications observed among surgical patients. Accumulating evidence suggests that neuroinflammation is one of the major contributors to the development of PNDs, but the underlying mechanisms remain unclear. METHODS: qPCR and ELISA analysis were used for detecting LCN2 and cytokine levels. cx3cr1CreER/-:: R26iDTR/- crossed mouse line was used for microglia depletion; intracranial injection of recombinant LCN2 (rLCN2) and adeno-associated viruses (AAV)-mediated shRNA silencing approaches were used for gain and loss of function, respectively. Combing with in vitro microglia cell culture, we have studied the role of LCN2 in surgery-induced cognitive decline in mice. RESULTS: We revealed that Lcn2 mRNA and protein levels were greatly increased in mouse hippocampal neurons after surgery. This surgery-induced elevation of LCN2 was independent of the presence of microglia. Gain of function by intracranial injection of rLCN2 protein into hippocampus disrupted fear memory in naive mice without surgery. Conversely, silencing LCN2 in hippocampus by AAV-shRNA protected mice from surgery-induced microglia morphological changes, neuroinflammation and cognitive decline. In vitro, application of rLCN2 protein induced the expression of several pro-inflammatory cytokines in both BV-2 and primary microglia culture. CONCLUSIONS: These data suggest LCN2 acts as a signal from neuron to induce proinflammatory microglia, which contributes to surgery-induced neuroinflammation and cognitive decline in mice.

Comparison of Postoperative Pain in 70 Women with Breast Cancer Following General Anesthesia for Mastectomy with and without Serratus Anterior Plane Nerve Block.

BACKGROUND [color=black]This study was conducted at a single center and aimed to compare postoperative pain in 70 women with breast cancer following general anesthesia for mastectomy with and without serratus anterior plane (SAP) block.[/color] MATERIAL AND METHODS [color=black]A total of 70 breast cancer patients who met the criteria were randomly divided into the general anesthesia combined with SAP block group (group S) and the general anesthesia only group (group G). Perioperative anesthetic drug dosage, the visual analog scale (VAS) score at different time points, and the patient's satisfaction with analgesia 24 h after surgery, and incidence of postmastectomy pain syndrome (PMPS) were statistically analyzed in the 2 groups.[/color] RESULTS [color=black]Compared with group G, group S had lower intraoperative remifentanil dosages (P=0.003), a lower total amount of sufentanil via analgesia pump during the 24-h postoperative period (P<0.001), and lower VAS scores at 2 h, 4 h, and 8 h after surgery, and the differences were significant (P<0.05). Compared with group G, group S had a shorter first flatus time, got out of bed sooner, had a lower incidence of nausea and vomiting (P<0.05), and lower incidence of PMPS at 3 and 6 months after the operation (P<0.05).[/color] CONCLUSIONS [color=black]At a single center, preoperative SAP block can significantly reduce postoperative pain after modified radical mastectomy for breast cancer.[/color].

Incidence and Associations of Acute Kidney Injury after General Thoracic Surgery: A System Review and Meta-Analysis.

(1) Background: Acute kidney injury (AKI) is related to adverse outcomes in critical illness and cardiovascular surgery. In this study, a systematic literature review and meta-analysis was carried out to evaluate the incidence and associations of AKI as a postoperative complication of thoracic (including lung resection and esophageal) surgical procedures. (2) Methods: Adopting a systematic strategy, the electronic reference databases (PubMed, EMBASE, and Cochrane Library) were searched for articles researching postoperative renal outcomes that were diagnosed using RIFLE, AKIN or KDIGO consensus criteria in the context of a thoracic operation. A random-effects model was applied to estimate the incidence of AKI and, where reported, the pooled relative risk of mortality and non-renal complications after AKI. The meta-analysis is registered in PROSPERO under the number CRD42021274166. (3) Results: In total, 20 studies with information gathered from 34,826 patients after thoracic surgery were covered. Comprehensively, the incidence of AKI was estimated to be 8.8% (95% CI: 6.7−10.8%). A significant difference was found in the mortality of patients with and without AKI (RR = 2.93, 95% CI: 1.79−4.79, p < 0.001). Additionally, in patients experiencing AKI, cardiovascular and respiratory complications were more common (p = 0.01 and p < 0.001, respectively). (4) Conclusions: AKI is a common complication associated with adverse outcomes following general thoracic surgery. An important issue in perioperative care, AKI should be considered as a highly significant prognostic indicator and an attractive target for potential therapeutic interventions, especially in high-risk populations.