Background:Renal ischemia-reperfusion injury (IRI) is an inevitable occurrence during kidney transplantation. Mitophagy, ferroptosis, and the associated immune microenvironment (IME) have been shown to play important roles in renal IRI. However, the role of mitophagy-associated IME genes in IRI remains unclear. In this study, we aimed to construct a prediction model of IRI prognosis based on mitophagy-associated IME genes.Method:The specific biological characteristics of the mitophagy-associated IME gene signature were comprehensively analyzed using public databases such as GEO, Pathway Unification, and FerrDb. Correlations between the expression of prognostic genes and immune-related genes and IRI prognosis were determined by Cox regression, LASSO analysis, and Pearson's correlation. Molecular validation was performed using human kidney 2 (HK2) cells and culture supernatant as well as the serum and kidney tissues of mice after renal IRI. Gene expression was measured by PCR, and inflammatory cell infiltration was examined by ELISA and mass cytometry. Renal tissue damage was characterized using renal tissue homogenate and tissue sections.Results:The expression of the mitophagy-associated IME gene signature was significantly correlated with IRI prognosis. Excessive mitophagy and extensive immune infiltration were the primary factors affecting IRI. In particular, FUNDC1, SQSTM1, UBB, UBC, KLF2, CDKN1A, and GDF15 were the key influencing factors. In addition, B cells, neutrophils, T cells, and M1 macrophages were the key immune cells present in the IME after IRI. A prediction model for IRI prognosis was constructed based on the key factors associated with the mitophagy IME. Validation experiments in cells and mice indicated that the prediction model was reliable and applicable.Conclusion:We clarified the relationship between the mitophagy-related IME and IRI. The IRI prognostic prediction model based on the mitophagy-associated IME gene signature provides novel insights on the prognosis and treatment of renal IRI.

A spiral interdigitated MXene-assisted field effect transistor (SiMFETs) was proposed for determination of IL-6 in patients with kidney transplantation infection. Our SiMFETs demonstrated enhanced IL-6 detection range of 10 fg/mL-100 ng/mL due to the combination of optimized transistor's structure and semiconducting nanocomposites. Specifically, on one hand, MXene-based field effect transistor drastically amplified the amperometric signal for determination of IL-6; on the other hand, the multiple spiral structure of interdigitated drain-source architecture improved the transconductance of FET biosensor. The developed SiMFETs biosensor demonstrated satisfactory stability for 2 months, and favorable reproducibility and selectivity against other biochemical interferences. The SiMFETs biosensor exhibited acceptable correlation coefficient (R2=0.955) in quantification of clinical biosamples. The sensor successfully distinguished the infected patients from the health control with enhanced AUC of 0.939 (sensitivity of 91.7%, specificity of 86.7%). Those merits introduced here may pave an alternative strategy for transistor-based biosensor in point-of-care clinic applications.

Significance Statement Hypoxia is a hallmark of renal ischemia-reperfusion injury (IRI) and serves as an essential regulator of innate immune responses during this process, although the mechanisms of this regulation remain unclear. Here, we showed in a murine model that HIF-2 α knockout in dendritic cells (DCs) exacerbated renal IRI through activation of natural killer T cells. Mechanistically, HIF-2 α deficiency upregulated CD36 expression of DCs, leading to cellular lipid accumulation. Pharmacologic inhibition of CD36 in DCs resulted in renoprotection by reducing lipid content and suppressing natural killer T cell activation. Our study strongly suggests that targeting the HIF-2 α /CD36 regulatory axis may be a strategy for alleviating renal IRI. Background Hypoxia and hypoxia-inducible factors (HIFs) play essential and multiple roles in renal ischemia-reperfusion injury (IRI). Dendritic cells (DCs) comprise a major subpopulation of the immunocytes in the kidney and are key initiators and effectors of the innate immune responses after IRI. The role of HIF-2 α in DCs remains unclear in the context of renal IRI. Methods To investigate the importance of HIF-2 α in DCs upon renal IRI, we examined the effects of DC-specific HIF-2 α ablation in a murine model. Bone marrow–derived DCs (BMDCs) from DC-specific HIF-2 α –ablated mice and wild-type mice were used for functional studies and transcriptional profiling. Results DC-specific ablation of HIF-2 α led to hyperactivation of natural killer T (NKT) cells, ultimately exacerbating murine renal IRI. HIF-2 α deficiency in DCs triggered IFN- γ and IL-4 production in NKT cells, along with upregulation of type I IFN and chemokine responses that were critical for NKT cell activation. Mechanistically, loss of HIF-2 α in DCs promoted their expression of CD36, a scavenger receptor for lipid uptake, increasing cellular lipid accumulation. Furthermore, HIF-2 α bound directly to a reverse hypoxia-responsive element (rHRE) in the CD36 promoter. Importantly, CD36 blockade by sulfo- N -succinimidyl oleate (SSO) reduced NKT cell activation and abolished the exacerbation of renal IRI elicited by HIF-2 α knockout. Conclusions Our study reveals a previously unrecognized role of the HIF-2 α /CD36 regulatory axis in rewiring DC lipid metabolism under IRI-associated hypoxia. These findings suggest a potential therapeutic target to resolve long-standing obstacles in treatment of this severe complication.

En bloc kidney transplantation (EBKT) to adults from preterm neonates following donation after circulatory death has not been described in the literature. We report 2 successful cases of EBKT from preterm neonatal donation after circulatory death donors weighing <1.2 kg to adult recipients. The first case was a preterm female infant born at 29 weeks' gestational age, weighing 1.07 kg. The recipient was a 34-year-old woman weighing 75 kg. At the 9-month follow-up, the patient demonstrated excellent graft function with a creatinine concentration of 1.48 mg/dL. The second donor was a preterm female infant born at 29 weeks and 5 days' gestation, weighing 1.17 kg. The recipient was a 25-year-old woman weighing 46 kg. By 5 months post surgery, the serum creatinine level had gradually decreased to 1.47 mg/dL. In our experience, EBKT from preterm neonates <30 weeks' gestation and weighing <1.2 kg has demonstrated acceptable short- to medium-term results.

Objective:To explore the correlation between post-transplant non-HLA antibodies and humoral rejection(HR)after kidney transplantation(KT).Methods:A retrospective study was conducted for KT recipients with non-HLA antibody level detected from September 2019 to January 2021.The recipients with biopsy confirmed HR and donor-specific HLA antibodies negative or feeble positive at the time of HR were designated as HR group while recipients with stable renal allograft function from 2 weeks post-KT to the time of detecting non-HLA antibody as stable group.The levels of HLA antibody, MHC classⅠchain-related gene A(MICA)antibody and 32 non-HLA antibodies were tested by Luminex single antigen bead and the levels of angiotensin Ⅱ type 1 receptor(AT1R)antibody quantified by enzyme-linked immunosorbent assay (ELISA). Inter-group differences in positive rate of non-HLA antibodies and number of positive non-HLA antibodies were analyzed.Results:Twenty-four recipients had positive non-HLA antibodies while the remainders had no positive non-HLA antibodies.Three HR recipients were positive for actin antibody, collagen Ⅲ antibody, glutathione S-transferase theta-1 antibody or IFN-γ antibody respectively.However, all four non-HLA antibodies of stable recipients were negative.There was significant inter-group difference( P=0.017). Four HR recipients were positive for collagenⅡantibody while only 1 stable recipient was positive for collagenⅡantibody.The positive rate of collagenⅡ antibody was significantly higher in HR recipients than that in stable recipients( P=0.023). HR recipients had an average of 2.36 positive non-HLA antibodies while stable recipients had an average of 0.90.There was significant inter-group difference ( P=0.008). Conclusions:A high level of non-HLA antibodies may elevate the risk of HR after KT.

Exosomes derived from mesenchymal stem cell (MSC) alleviate kidney damage through autophagy. This study determined whether MSCs relieve renal fibrosis and inhibit autophagy by exosome transfer of miRNA-122a. The gene expression involved in the mTOR signaling pathway and autophagy was assessed in TGF-β1-treated human renal tubular epithelial cells (HK-2) and unilateral ureteral obstruction (UUO) mice before and after MSC-derived exosomes and miRNA-122a mimic treatment. Small RNA (sRNA) next-generation sequencing was also performed on TGF-β1-treated HK-2 cells. MSC-derived exosomes relieve fibrosis caused by TGFβ in HK-2 via regulation of the mTOR signaling pathway and downstream autophagy. Furthermore, we found that MSC-derived exosomes mediate miRNA-122a to relieve renal fibrosis in HK-2 cells in response to TGF-β1 through the regulation of mTOR signaling and autophagy. In the UUO mouse model, miRNA-122a mimic-transfected MSC treatment and its combination with 3-MA both recapitulated the same results as the in vitro experiments, along with reduced expansion of renal tubule, interstitial expansion, and preservation of kidney architecture. The antifibrotic activity of MSC-derived exosomes after renal fibrosis occurs partially by autophagy suppression via excreted exosomes containing mainly miRNA-122a. These findings indicate that the export of miRNA-122a via MSC-derived exosomes represents a novel strategy to alleviate renal fibrosis.

OBJECTIVES:To evaluate the efficacy and safety of low-dose trimethoprim (TMP)-sulfamethoxazole (SMX) (TMP-SMX) as the primary prophylaxis for Pneumocystis jirovecii pneumonia (PJP) in adult recipients of kidney transplantation.METHODS:Three kinds of prescriptions in kidney recipients were documented, including 20 mg TMP/100 mg SMX oral daily, 20 mg TMP/100 mg SMX oral every other day, and nonprophylaxis. The primary outcome was the incidence of PJP in the first 180 days of follow-up after kidney transplantation. The secondary outcomes were changes in renal and liver function.RESULTS:Among the 1469 recipients, 1066 (72.56%) received 20 mg TMP/100 mg SMX daily, 127 (8.65%) received 20 mg TMP/100 mg SMX every other day, and 276 (18.79%) did not have prophylaxis prescription. The 276 recipients in the nonprophylaxis group had 124.92 person-years of follow-up, during which PJP occurred in 29 patients, for an incidence rate of 23.21 (95% confidence interval 15.76-32.72) per 100 person-years. The TMP-SMX daily group and the TMP-SMX every other day group had 524.89 and 62.07 person-years of follow-up, respectively, with no occurrence of PJP. There was no significant difference among the three groups in changes in renal and liver function (P >0.05, respectively). A total of 111 recipients in each group were enrolled in the propensity score matching analysis. It was revealed that the 111 nonprophylaxis recipients had 51.27 person-years of follow-up and 10 PJP cases. Prophylaxis was considered effective because there was a significant difference between the three groups (P <0.001).CONCLUSION:Low-dose TMP-SMX prophylaxis significantly reduces the incidence of PJP within 6 months after kidney transplantation and has a favorable safety profile.

The aim of the present study is to build a software implementation of a previous study and to diagnose discoid lateral menisci on knee joint radiograph images. A total of 160 images from normal individuals and patients who were diagnosed with discoid lateral menisci were included. Our software implementation includes two parts: preprocessing and measurement. In the first phase, the whole radiograph image was analyzed to obtain basic information about the patient. Machine learning was used to segment the knee joint from the original radiograph image. Image enhancement and denoising tools were used to strengthen the image and remove noise. In the second phase, edge detection was used to quantify important features in the image. A specific algorithm was designed to build a model of the knee joint and measure the parameters. Of the test images, 99.65% were segmented correctly. Furthermore, 97.5% of the tested images were segmented correctly and their parameters were measured successfully. There was no significant difference between manual and automatic measurements in the discoid (P=0.28) and control groups (P=0.15). The mean and standard deviations of the ratio of lateral joint space distance to the height of the lateral tibial spine were compared with the results of manual measurement. The software performed well on raw radiographs, showing a satisfying success rate and robustness. Thus, it is possible to diagnose discoid lateral menisci on radiographs with the help of radiograph-image-analyzing software (BM3D, etc.) and artificial intelligence-related tools (YOLOv3). The results of this study can help build a joint database that contains data from patients and thus can play a role in the diagnosis of discoid lateral menisci and other knee joint diseases in the future.

Renal ischemia/reperfusion injury (IRI) is the major cause of acute kidney injury. However, mechanisms underlying the sudden loss in kidney function and tissue injury remain to be fully elucidated. Here, we performed RNA sequencing to systematically compare the transcriptome differences between IR injured kidneys and sham kidneys. We observed that mitochondrial dynamics was destructed in renal IRI. Expression of mitochondrial fusion-associated genes was reduced, whereas expression of mitochondrial fission-related genes was increased in renal IRI, and these findings were further confirmed by mitochondrial morphological observations. By screening 19 purinergic receptors, we noticed that P2RX1 expression was markedly upregulated in renal IRI. RNA sequencing and mitochondrial morphological observations revealed that mitochondrial dynamics was preserved in P2RX1 genetic knockout (P2rx1-/-) mice. Neutrophil extracellular traps (NETs) were reported to be essential for tissue injury in renal IRI, but the detailed mechanism remained unclear. In the present study, we found that P2RX1 favored the formation of neutrophil extracellular traps (NETs) in IRI, and NETs was essential for the impairment of mitochondrial dynamics. Mechanistically, P2RX1-involved metabolic interaction between platelets and neutrophils supported NETs formation. Activation of P2RX1 promoted platelets ATP release, which subsequently contributed to neutrophil glycolytic metabolism and NETs generation.

Significant variation in impedance under a wide range of loads increases the difficulty of frequency tracking and vibration control in high-power piezoelectric systems (HPPSs). This paper proposed a wide operating range driving and control scheme for HPPSs. We systematically analyzed the impedance characteristics and deduced the load optimization frequency. In order to provide sufficient drive capability, the inverter combined with an LC matching circuit is configured. With the aid of a transformer ratio arm bridge (TRAB) combined with a proposed pulse-based phase detector (PBPD), the proposed scheme can control the vibration amplitude and keep parallel resonance status under a wide range of loads. Experiments conducted under actual operating conditions verify the feasibility of the proposed scheme under the modal resistance range from 7.40 to 500 Ω and the vibration range from 20% to 100%. Moreover, with the aid of a laser displacement sensor, our scheme is verified to have a vibration amplitude control accuracy better than 2% over a tenfold load variation. This research could be helpful for the driving and control of HPPSs operating in a wide range.

Objective To explore the rapid diagnosis and clinic treatment of donor-derived carbapenem-resistant Klebsiella pneumoniae (CRKP) infection in renal transplant recipients .Methods Retrospective analysis was performed for clinical data and the diagnosis and treatment of 9 renal transplant recipients with donor-derived CRKP infection from March 2017 to May 2019 .Results Among 526 renal transplant recipients ,nine were diagnosed with donor-derived CRKP infection by bacterial culture or KPC enzyme gene test .The infection rate was 1 .71％ .One recipient receiving carbapenem and tigecycline died while the remainders survived after a treatment of ceftazidime-avibactam and carbapenem . One recipient underwent graft resection . Among 8 recipients on ceftazidime-avibactam ,5 cases received a standard dose of 3 .75 g/d while another 3 cases had a high dose of 7 .5 g/d .One patient in standard-dose group underwent graft resection due to an arteriorrhexis of artery anastomosis .After graft resection ,the patient received a high dose of ceftazidime-avibactam and survived to date .The grafts of three patients in high-dose treatment group survived .Conclusions KPC enzyme gene detection plus injecting lavage fluid into blood culture bottle for bacterial culture is rapid and accurate for diagnosing donor-derived CRKP infection . A combination of ceftazidime-avibactam plus carbapenem is effective for donor-derived CRKP infection .A high dose of ceftazidime-avibactam may improve the efficacy without obvious side effects .

The contribution of glycogen synthase kinase‐3β (GSK‐3β) to cholestatic liver disease (CLD) remains unknown. We investigated the role and mechanism of GSK‐3β in vivo in liver tissues of patients with CLD and the bile duct ligation (BDL) mouse model and in vitro using a hepatic progenitor cell (HPC) and hepatic stellate cell (HSC) coculture system. In liver tissues of patients with CLD, expression of the inactive form of GSK‐3β, phospho‐GSK‐3β(Ser9), was increased in HPCs. GSK‐3β inhibition by SB216763 treatment aggravated liver fibrosis and elevated the expression of osteopontin (OPN) in the BDL mouse model. OPN was significantly overexpressed in liver tissues and serum from patients with CLD. In an HPC and HSC coculture system, inhibition of GSK‐3β induced OPN production, which activated HSCs in a cholestatic environment. The expression of activator protein 1 (AP‐1), an important downstream transcription factor of GSK‐3β, was significantly increased in liver tissues of patients with CLD and SB216763‐treated BDL mice. Finally, OPN expression was directly modulated by AP‐1. These observations indicate that GSK‐3β inhibition up‐regulates OPN expression via AP‐1 activation, which accelerates the progression of cholestatic liver fibrosis in patients with CLD and in BDL mice.—Zhuang, S., Hua, X., He, K., Zhou, T., Zhang, J., Wu, H., Ma, X., Xia, Q., Zhang J. Inhibition of GSK‐3β induces AP‐1‐mediated osteopontin expression to promote cholestatic liver fibrosis. FASEB J. 32, 4494–4503 (2018). www.fasebj.org

目的 探讨肾移植供者来源耐药肺炎克雷伯杆菌感染的临床特点,总结临床治疗经验.方法 回顾性分析2016年1月-2017年10月上海市3家肾移植中心13例术后发生供者来源耐药肺炎克雷伯杆菌感染的受者临床资料.结果 13例受者中,1例为供体血管培养阳性,12例为供体肾脏灌洗液培养阳性.13例受者中,5例未使用阿维巴坦治疗,均引起广泛移植肾周耐药肺炎克雷伯杆菌感染,导致受者死亡;1例术后移植肾周引流液培养持续阳性,应用头孢他啶-阿维巴坦和碳青霉烯类药物联合治疗后痊愈;6例术后供体肾脏灌洗液培养为阳性时,即开始应用头孢他啶-阿维巴坦和碳青霉烯类药物联合治疗,均治愈.1例术后供肾动脉培养为阳性,应用头孢他啶-阿维巴坦治疗后引流液未培养出细菌,患者长期存活.结论 头孢他啶-阿维巴坦联合碳青霉烯类药物联合治疗移植肾供体来源耐药肺炎克雷伯杆菌感染效果确切,且未见明显不良反应.供肾灌洗液培养阳性时,应及早干预,保障患者安全.

Integrating ultrasonic power supply with Ethernet technologies, monitoring and controlling parameters could reduce overhaul interval and pecuniary loss for producers. However, how to add new features to the system without reducing the controlling frequency of the microcontroller is a problem. This article proposes a new architecture of ultrasonic power supply with dual microcontrollers cooperating, and invents a new method of dual communication through Serial Peripheral Interface at over 2000Hz frequency. Then developing a web-based communication system with Ethernet Technology and LwIP protocol stack to monitor and adjust parameters. The experimental result shows that both microcontrollers has enough operational capability for all tasks, and technicians could remotely keep watch on real-time parameters and adjust control parameters to avoid wrong working situations.

Oxidative stress has a critical role in the pathogenesis of acetaminophen (APAP) induced hepatocellular necrosis, and the identification of novel approaches to attenuate oxidative stress is essential to prevent/revert the disease. This study investigated the role of both HIF-1 and HIF-2 in the pathogenesis of APAP-induced oxidative stress, as well as the underlying mechanisms. In the present study, we initially found that knockout of HIF-1α or HIF-2α reduced APAP toxicity, and double knockout afforded the best protection. APAP treatment led to stabilization of both HIF-1α and HIF-2α in mouse livers. Moreover, the protective effects of HIF deficiency were related to the attenuated oxidative stress. Further experiments proved that PPARα, a master regulator in cellular metabolism accounted for the HIF deficiency-caused protective impact on APAP toxicity. Inactivation of HIFs promoted the expression of peroxisome proliferator-activated receptor α (PPARα) in the liver, which in turn activated nuclear factor erythroid 2-related factor 2 (Nrf2). Knockdown of PPARα or Nrf2 negated the hepatoprotection afforded by HIF deficiency. At last，examination of the PPARα promoter identified a HIF-binding site and HIF-dependent repression of PPARα in hepatocytes by luciferase reporter and EMSA study. Taken together， Our results demonstrate that HIFs are key suppressors of PPARα in the liver, thereby compromising the adaptive defense mechanisms against oxidative stress when confronted with APAP. These findings are important to the etiology and therapeutics of APAP hepatotoxicity. The functional link between HIFs and PPARα may have more implications in liver physiology and other pathologic conditions than APAP injury.

Background/Aims: This study aimed to evaluate the effects of exosomes produced by human-induced pluripotent stem cell-derived mesenchymal stromal cells (hiPSC-MSCs-Exo) on hepatic ischemia-reperfusion (I/R) injury, as well as the underlying mechanisms. Methods: Exosomes derived from hiPSC-MSCs were isolated and characterized both biochemically and biophysically. hiPSC-MSCs-Exo were injected systemically into a murine ischemia/reperfusion injury model via the inferior vena cava, and then the therapeutic effects were evaluated. The serum levels of transaminases (aspartate aminotransferase (AST) and alanine aminotransferase (ALT), as well as histological changes were examined. Primary hepatocytes and human hepatocyte cell line HL7702 were used to test whether exosomes could induce hepatocytes proliferation in vitro. In addition, the expression levels of proliferation markers (proliferation cell nuclear antigen, PCNA; Phosphohistone-H3, PHH3) were measured by immunohistochemistry and Western blot. Moreover, SK inhibitor (SKI-II) and S1P1 receptor antagonist (VPC23019) were used to investigate the role of sphingosine kinase and sphingosine-1-phosphate-dependent pathway in the effects of hiPSC-MSCs-Exo on hepatocytes. Results: hiPSCs were efficiently induced into hiPSC-MSCs that had typical MSC characteristics. hiPSC-MSCs-Exo had diameters ranging from 100 to 200 nm and expressed exosome markers (Alix, CD63 and CD81). After hiPSC-MSCs-Exo administration, hepatocyte necrosis and sinusoidal congestion were markedly suppressed in the ischemia/reperfusion injury model, with lower histopathological scores. The levels of hepatocyte injury markers AST and ALT were significantly lower in the treatment group compared to control, and the expression levels of proliferation markers (PCNA and PHH3) were greatly induced after hiPSC-MSCs-Exo administration. Moreover, hiPSC-MSCs-Exo also induced primary hepatocytes and HL7702 cells proliferation in vitro in a dose-dependent manner. We found that hiPSC-MSCs-Exo could directly fuse with target hepatocytes or HL7702 cells and increase the activity of sphingosine kinase and synthesis of sphingosine-1-phosphate (S1P). Furthermore, the inhibition of SK1 or S1P1 receptor completely abolished the protective and proliferative effects of hiPSC-MSCs-Exo on hepatocytes, both in vitro and in vivo. Conclusions: Our results demonstrated that hiPSC-MSCs-Exo could alleviate hepatic I/R injury via activating sphingosine kinase and sphingosine-1-phosphate pathway in hepatocytes and promote cell proliferation. These findings represent a novel mechanism that potentially contributes to liver regeneration and have important implications for new therapeutic approaches to acute liver disease.

Background/Aims: Ischemia/reperfusion injury (IRI) plays a crucial role in renal transplantation and can cause renal failure associated with pyroptosis, a pro-inflammatory-induced programmed cell death. Small endogenous non-coding RNAs have been shown to be involved in renal ischemia/reperfusion injury. This study was performed to investigate which miRNAs regulate pyroptosis in response to renal ischemia/reperfusion injury and determine the mechanism underlying this regulation. Methods: An in vivo rat model of renal IRI was established, and the serum and kidneys were harvested 24 h after reperfusion to assess renal function and histological changes. For the in vitro study, the cultured human renal proximal tubular cell line HK-2 was subjected to 24 h of hypoxia (5% CO2, 1% O2, and 94% N2) followed by 12 h of reoxygenation (5% CO2, 21% O2, and 74% N2). The mRNA expression levels were analyzed by real-time PCR, and the protein expression levels were analyzed using Western blot, immunofluorescence staining and enzyme-linked immunosorbent assay (ELISA). Bioinformatics analyses were applied to predict miR-155 targets, which were then confirmed by a luciferase reporter assay. Results: We found that the levels of pyroptosis-related proteins, including caspase-1, caspase-11, IL-1β and IL-18, were significantly increased after renal ischemia/reperfusion injury. Similarly, hypoxia-reoxygenation injury (HRI) also induced pyroptosis in HK2 cells. Furthermore, our study revealed that miR-155 expression was substantially increased in the renal tissues of IRI rats and in HRI HK2 cells. Up-regulation of miR-155 promoted HK2 cell pyroptosis in HRI; conversely, knockdown of miR-155 attenuated this process. To understand the signaling mechanisms underlying the pro-pyroptotic activity of miR-155, we found that exogenous expression of miR-155 up-regulated the expression of caspase-1 as well as the pro-inflammatory cytokines IL-1β and IL-18. Moreover, miR-155 directly repressed FoxO3a expression and its downstream protein apoptosis repressor with caspase recruitment domain (ARC). Conclusions: Our study proposes a new signaling pathway of miR-155/FoxO3a/ARC leading to renal pyroptosis under ischemia/reperfusion injury conditions.