Acute kidney injury (AKI), triggered by various stimuli including ischemia-reperfusion, nephrotoxic insult, and sepsis, is characterized by an abrupt deterioration in kidney function. Ubiquitination is a post-translational modification of proteins that plays a critical role in the pathogenesis and progression of AKI. In this study, we aimed to investigate the role and underlying mechanism of the deubiquitinating enzyme Josephin Domain-containing protein 2 (JOSD2) in AKI. We found that deficiency of JOSD2 exacerbated renal tubular injury and inflammation in AKI mice induced by cisplatin or ischemia-reperfusion injury. Conversely, the specific overexpression of JOSD2 in renal tubular epithelial cells effectively prevented renal tubular injury and inflammation induced in AKI mice. Mechanistically, we identified Sirtuin 7 (SIRT7) as a potential substrate of JOSD2 through mass spectrometry combined with co-immunoprecipitation analysis. JOSD2 removes the K63-linked ubiquitination of SIRT7 via its active site C24 and promotes P62-mediated autophagic degradation of SIRT7, which subsequently prevents the phosphorylation and nuclear translocation of P65 and reduces inflammatory responses in renal tubular epithelial cells. Our study reveals the role of the JOSD2-SIRT7 axis in regulating AKI-induced renal inflammation and highlights the potential of JOSD2 as a promising therapeutic target for AKI.

AimThe objective of this study is to investigate the influence of various components, viscosity, ultrasonic frequency, and depth of the region of interest on Young’s modulus of the viscoelastic model.MethodsViscoelastic models, characterized by distinct viscosities and compositions, were fabricated using gelatin as the elastomeric component, fructose as the viscous component, and milk powder as an additive ingredient. Shear wave elastography (SWE) technology was utilized, with the acoustic frequencies set at 7 MHz, 8 MHz, and 9 MHz, respectively. Additionally, the depths of regions of interest (ROI) were varied at 1 cm, 2 cm, and 3 cm to enable a comparison of Young’s modulus values across different viscoelastic body models.ResultsIn order to generate viscoelastic models with varying compositions, gelatin samples with the same concentration were prepared with different concentrations of fructose added. Under consistent frequency and ROI depth conditions, no statistically significant differences were observed in the measured Young’s modulus values among these models (p > 0.05). However, for models composed solely of gelatin, significant differences in Young’s modulus values were noted at varying sound wave frequencies and ROI depths (p < 0.05). When samples with different fructose and powdered milk compositions and concentrations were prepared at a constant gelatin concentration, a range of viscoelastic models with diverse properties was created. Analysis of the Young’s modulus values at varying sound wave frequencies and ROI depths revealed a statistically significant difference for all model groups when the frequency was 8 MHz and the ROI depth was 3 cm. Moreover, using linear regression analysis on these models after the addition of powdered milk showed that frequency had a significantly negative impact on the Young’s modulus, with a regression coefficient of −0.488 (t = −7.341, p < 0.01), while depth demonstrated a significantly positive influence on the shear modulus, with a regression coefficient of 0.480 (t = 7.158, p < 0.01).ConclusionThe self-constructed viscoelastic model demonstrates convenience and adaptability, allowing flexible control over its viscosity and composition. Under varying conditions, the factors determining Young’s modulus differ; elements such as compositional heterogeneity, frequencies, and ROI depth all influence the modulus.

The three-dimensional structures of proteins are being solved apace, yet this information is often underused in quantitative structure-activity relationship (QSAR) studies. Here, we describe and compare methods for exploiting protein structures to derive 3D-QSARs. These methods can facilitate molecular design and lead optimization and should increasingly become a standard component of the drug designer's repertoire.:

BACKGROUND:We sought to evaluate renal stiffness in children with hematuria and/or proteinuria using shear wave elastography (SWE) and to investigate the clinical value of renal stiffness in children with hematuria and/or proteinuria. METHODS:According to the results of urinary occult blood and urinary protein tests, 349 pediatric patients were categorized into one of four groups: pure hematuria (HU), pure proteinuria (PU), concomitant hematuria and proteinuria (HUPU), or control (non-HUPU). Patient demographic data, laboratory test results, and renal ultrasound data were collected. RESULTS:There were significant differences in cortical/medullary elasticity among the four groups (the most sensitive cutoff value between HU and PU was 1.72) (P < 0.05). We found that hematuria and proteinuria interacted with renal cortical elasticity (P < 0.05) but that hematuria and proteinuria did not interact with renal medullary elasticity or cortical/medullary elasticity (P > 0.05). Renal elasticity values correlated with sex, age, body surface area, body mass index, qualitative urinary protein, urine N-acetyl-β-D-glucosaminidase, 24-hour urinary protein quantity, renal volume, and renal cortical thickness (P < 0.05). CONCLUSIONS:SWE can be used to detect changes in renal stiffness in children with hematuria and/or proteinuria. SWE is beneficial for the early detection of glomerular disease in children with abnormal urine test results. IMPACT:This study evaluated the utility of shear wave elastography for the assessment of renal elasticity in pediatric patients presenting with hematuria and/or proteinuria. Children with pure proteinuria had significantly higher renal cortical/medullary elasticity values than those with pure hematuria. An interaction effect between hematuria and proteinuria on renal cortical stiffness was observed. Shear wave elastography can be used as a tool to assess early renal injury in children with urinalysis abnormalities.

Objective To explore the value of shear wave elastography(SWE)in the kidneys of children with Henoch-Schonlein purpura(HSP).Methods A total of 59 cases with HSP admitted to the Second Affiliated Hospital of Wenzhou Medical University from November 2021 to August 2022 were selected and divided into simple HSP group(29 cases)and Henoch-Schonlein purpura nephritis(HSPN)group(30 cases).50 normal children during the same period were included as control group.The Young′s modulus(YM)of right renal cortex and medulla were compared among the three groups.receiver operating characteristic curve(ROC curve)was plotted to evaluate the diagnostic efficiency of SWE for simple HSP.Correlation analysis and multiple linear regression analysis were performed for the YM value of right renal cortex and medulla of all children with HSP and related indexes.Results There was statistical significance in YM values of right renal cortex and medulla among the three groups(P<0.05).The YM value of right renal cortex of the simple HSP group was higher than that in the control group and HSPN group(P<0.05).The YM value of right renal medulla of the simple HSP group were higher than that in the control group(P<0.05).The YM value of right renal cortex was better than the YM value of right renal medulla in the diagnostic efficiency of simple HSP.The YM value of right renal cortex and medulla both had a linear regression relation-ship with the right renal volume.Conclusion The YM value of right renal cortex and medulla were higher than those of healthy children,with the progression of the disease the YM values decreasing.It may become a new technology for routine screening and follow-up moni-toring of renal involvement in children with HSP.

Background: The virtual touch quantification (VTQ) using acoustic radiation force impulse (ARFI) is a type of ARFI technology, which has been widely used against many diseases. The sensitivity and specificity of VTQ in differentiating immunoglobulin A nephropathy (IgAN) patients from healthy controls remain unestablished. Objectives: The present study aimed to measure the VTQ values of renal parenchyma in patients with IgAN and to evaluate the efficacy of these values in distinguishing IgAN patients from healthy individuals. Patients and Methods: Ultrasound examinations were performed for the experimental and control groups. All routine ultrasound data, including the renal parenchymal thickness, renal volume, resistive index (RI) of interlobar renal arteries, and peak velocity of interlobar renal arteries, were collected. The VTQ values were measured in the middle and lower renal parenchyma using the VTQ technique. A receiver operating characteristic (ROC) curve was plotted to evaluate the efficacy of VTQ in differentiating IgAN patients from healthy individuals. Results: The VTQ values, RI values of interlobar arteries, and peak velocity of interlobar arteries were significantly different between patients with IgAN and the controls (2.14 ± 0.31 vs. 2.62 ± 0.24 m/s, 0.68 ± 0.05 vs. 0.63 ± 0.03 m/s, and 0.56 ± 0.59 vs. 0.60 ± 0.58 m/s; P < 0.05 for all). The VTQ values were associated with the renal parenchymal thickness, peak flow velocity of interlobular arteries, and Lee’s grade (P < 0.05 for all). The ROC curve analysis revealed that VTQ values might be used as a diagnostic method for differentiating IgAN patients (area under the curve [AUC] = 0.909) from healthy controls. Conclusion: The VTQ values significantly decreased in patients with IgAN and might play an important role in distinguishing IgAN patients from healthy individuals, with high sensitivity and specificity.

目的 探讨剪切波弹性成像(SWE)技术对评价健康儿童肾脏皮质弹性定量研究的临床价值,为儿童肾脏疾病的诊断及鉴别诊断提供重要的参考依据.方法 回顾性分析200例接受体检的健康儿童.所有受检者均采集一般临床资料、二维超声、彩色多普勒超声及剪切波弹性肾脏成像等参数,对不同年龄段肾皮质平均杨氏模量值与临床资料和二维及超声测量参数进行比较,同时分析这些参数与肾脏皮质硬度的相关性.结果 不同年龄组右肾中部皮质平均杨氏模量值参数比较差异有统计学意义(P＜0.01),婴幼儿组右肾中部皮质平均杨氏模量值最低.对侧左侧结果亦相同.同侧肾脏大小间肾皮质平均杨氏模量值差异有统计学意义.肾皮质平均杨氏模量值与年龄、身高、体表面积、肾脏体积大小、肾动脉主干血流峰值流速、肾动脉主干血流舒张末期流速有一定相关性,呈正相关(r = 0.142,P = 0.04;r = 0.202,P=0.004;r = 0.232,P = 0.007;r = 0.160,P = 0.023;r = 0.143,P = 0.027;r = 0.153,P = 0.023),与体表面积参数值相关性最好.结论 剪切波弹性成像可用于定量评价健康儿童的肾皮质杨氏模量值,为临床提供参考依据.

Rationale: Understanding the molecular mechanisms of deleterious cardiac remodeling is important for the development of treatments for heart failure. Recent studies have highlighted a role of deubiquitinating enzymes in cardiac pathophysiology. In the present study, we screened for alteration of deubiquitinating enzymes in experimental models of cardiac remodeling, which indicated a potential role of OTU Domain-Containing Protein 1 (OTUD1). Methods: Wide-type or OTUD1 knockout mice with chronic angiotensin II infusion and transverse aortic constriction (TAC) were utilized to develop cardiac remodeling and heart failure. We also overexpressed OTUD1 in mouse heart with AAV9 vector to validate the function of OTUD1. LC-MS/MS analysis combined with Co-IP was used to identify the interacting proteins and substrates of OTUD1. Results: We found that OTUD1 is elevated in mouse heart tissues following chronic angiotensin II administration. OTUD1 knockout mice were significantly protected against angiotensin II-induced cardiac dysfunction, hypertrophy, fibrosis and inflammatory response. Similar results were obtained in the TAC model. Mechanistically, OTUD1 bounds to the SH2 domain of STAT3 and causes deubiquitination of STAT3. Cysteine at position 320 of OTUD1 exerts K63 deubiquitination to promote STAT3 phosphorylation and nuclear translocation, thereby increasing STAT3 activity to induce inflammatory responses, fibrosis, and hypertrophy in cardiomyocytes. Finally, OTUD1 overexpression by AAV9 vector increases Ang II-induced cardiac remodeling in mice and OTUD1-regulated responses can be inhibited by blocking STAT3. Conclusion: Cardiomyocyte OTUD1 promotes pathological cardiac remodeling and dysfunction by deubiquitinating STAT3. These studies have highlighted a novel role of OTUD1 in hypertensive heart failure and identified STAT3 as a target of OTUD1 in mediating these actions.

目的 评价声辐射力脉冲成像技术测量颈肩部疼痛患者斜方肌弹性值的可重复性.方法 选取2019年4月至2020年8月该院超声科门诊接受斜方肌弹性检测的42例颈肩部疼痛患者为研究对象,由两位超声医师分别测量不同时间的斜方肌弹性值.评价同一检查者不同时间测量的弹性值和不同检查者测量的弹性值的可重复性.结果 同一检查者在不同时间测量的斜方肌弹性值和不同检查者测量的斜方肌弹性值比较,差异无统计学意义(P＞0.05).斜方肌弹性值在同一检查者不同时间和不同检查者之间的组内相关系数(ICC)＞0.75及相关系数|r|＞0.80(P＜0.05).同时,Bland-Altman图显示斜方肌弹性值在检查者内的一致性和检查者间的可重复性良好.结论 该技术检测斜方肌弹性具有良好的可重复性.

The studies of the effect of diabetes on the stiffness of Achilles tendon (AT) tissue remain inconclusive, we believe it is necessary to find a reliable method which can be used to detect the stiffness changes of the AT in the diabetic state. The objective of the present study was to investigate the effectiveness of sound touch elastography (STE) as a tool for detecting diabetic Achilles tendinopathy. We conducted a retrospective review of 180 participants, consisting of 82 patients with type 2 diabetes mellitus (T2DM) and 98 healthy adults, who had undergone AT ultrasonography. Young ‘s modulus (E) values of the distal, middle, and proximal segments of bilateral ATs of all participants were measured using STE technique. The E values of each AT segment between the case and control group were compared. The E values of the three segments of ATs in T2DM patients were lower than the healthy controls (P < 0.05). In both groups, the E values of the distal segments were lower than those of the middle segments, and the latter were lower than those of the proximal segments (P < 0.05). The E value of each segment of AT was inversely related to FPG, HbA1c, and diabetes duration (P < 0.05). The best cut-off points for the E values of the three segments of the AT for detecting diabetic tendinopathy were 347.44 kPa (AUC, 0.779), 441.57 kPa (AUC, 0.692), and 484.35 kPa (AUC, 0.676), respectively. STE can be used as a complementary diagnostic tool for the diagnosis of diabetic Achilles tendinopathy.

Background: Heart failure is a common event in the course of hypertension. Recent studies have highlighted the key role of the non-hemodynamic activity of angiotensin II (Ang II) in hypertension-related cardiac inflammation and remodeling. A naturally occurring compound, diacerein, exhibits anti-inflammatory activities in various systems. Hypothesis/Purpose: In this study, we have examined the potential effects of diacerein on Ang II-induced heart failure. Methods: C57BL/6 mice were administered Ang II by micro-osmotic pump infusion for 4 weeks to develop hypertensive heart failure. Mice were treated with diacerein by gavage for final 2 weeks. RNA-sequencing analysis was performed to explore the potential mechanism of diacerein. Results: We found that diacerein could inhibit inflammation, myocardial fibrosis, and hypertrophy to prevent heart dysfunction, without the alteration of blood pressure. To explore the potential mechanism of diacerein, RNA-sequencing analysis was performed, indicating that MAPKs/c-Myc pathway is involved in that cardioprotective effects of Diacerein. We further confirmed that diacerein inhibits Ang II-activated MAPKs/c-Myc pathway to reduce inflammatory response in mouse hearts and cultured cardiomyocytes. Deficiency of MAPKs or c-Myc in cardiomyocytes abolished the anti-inflammatory effects of diacerein. Conclusion: Our results indicate that diacerein protects hearts in Ang II-induced mice through inhibiting MAPKs/c-Myc-mediated inflammatory responses, rendering diacerein a potential therapeutic candidate agent for hypertensive heart failure.

目的 探讨2型糖尿病(T2DM)患者肾实质硬度与尿蛋白成分的相关性.方法 选取2020年4-12月于该院住院的T2DM患者117例,应用声触诊组织定量技术(VTQ)测量患者的肾实质剪切波速度(SWV),同时收集患者一般临床资料如病程、年龄、血压;常规超声参数如左肾大小、肾实质厚度;肾功能指标如血肌酐、血清尿素氮及24 h尿蛋白定量;尿蛋白成分如α1-微球蛋白(α1-MG)、β2-微球蛋白(β2-MG)、免疫球蛋白、转铁蛋白和微量白蛋白,并计算各种尿蛋白占尿蛋白总量的百分比.应用SPSS22.0统计软件对数据进行统计分析.结果 肾实质SMV与糖尿病病程呈正相关(r=0.304,P<0.05).肾实质SWV与血肌酐、血清尿素氮及24 h尿蛋白定量呈负相关(r=-0.356、-0.281、-0.202,P<0.05).肾实质SWV与α1-MG、β2-MG百分比呈负相关(r=-0.611、-0.578,P<0.05).结论 T2DM患者肾实质SWV与尿液中小分子蛋白百分比密切相关,二者联合应用或将在糖尿病肾病诊断和疗效评估中发挥重要作用.

Hyperglycemia-associated inflammation contributes to diabetic cardiomyopathy. Myeloid differentiation primary-response protein 88 (MyD88) is an adapter protein of many Toll-like receptors (TLRs) and is recruited to TLRs to initiate inflammatory response in endotoxin-activated innate immunity. However, the role of MyD88 in diabetic cardiomyopathy is unknown. We examined the role and mechanism of MyD88 in inflammatory heart injuries in diabetes and identified MyD88 as a potential target for the treatment of diabetic cardiomyopathy. In this study, we first found that MyD88 expression was increased in cardiomyocytes of diabetic mouse hearts. In cultured cardiomyocytes, MyD88 inhibition either by siRNA or by small-molecular inhibitor LM8 markedly blocked TLR4-MyD88 complex formation, reduced pro-inflammatory mitogen-activated protein kinases/nuclear factor-κB (MAPKs/NF-κB) cascade activation and decreased pro-inflammatory cytokine expression under high glucose condition. Moreover, pharmacologic inhibition of MyD88 by LM8 showed significantly anti-inflammatory, anti-hypertrophic and anti-fibrotic effects in the hearts of both type 1 and type 2 diabetic mice. These beneficial effects of MyD88 inhibition were correlated to the reduced activation of TLR4-MyD88-MAPKs/NF-κB signaling pathways in the hearts. Taken together, MyD88 in cardiomyocytes mediates diabetes-induced cardiac inflammatory injuries and pharmacological inhibition of MyD88 shows significantly cardioprotective effects, indicating MyD88 as a potential therapeutic target for diabetic cardiomyopathy.

目的 探讨三维能量多普勒超声(3D-PDU)及其定量参数对预测子痫前期的应用价值.方法 应用三维能量多普勒超声成像对328例11 ～14周进行常规超声检查的孕妇胎盘血流灌注情况进行前瞻性观察分析,应用三维多普勒直方图计算胎盘血管指数(VI)、血流指数(FI)、血管和血流指数(VFI).所有患者在16～20周之间再进行一次检查.孕妇随访至分娩结束,按有无发生子痫前期分为正常妊娠组和子痫前期组.结果 16～ 20周子痫前期组胎盘血管指数(VI)、血流指数(FI)、血管和血流指数(VFI)等胎盘血管指数明显低于对照组.11～14周子痫前期组胎盘血管指数与对照组差异无统计学意义.结论 三维能量多普勒超声可定量分析胎盘血流灌注情况,可以预测及诊断子痫前期.

Curcumin (Cur) encapsulation in nanocapsules (NCs) could improve its availability and therapeutic antitumor efficacy. Cur-loaded chitosan/perfluorohexane (CS/PFH) nanocapsules (CS/PFH-Cur-NCs) were thus synthesized via a nanoemulsion process. To further enhance the selective tumor targeting ability of Cur-loaded NCs, a novel CS/PFH-Cur-NCs with conjugation of Arg-Gly-Asp (RGD) peptide (RGD-CS/PFH-Cur-NCs) were prepared in this study. The properties of these NCs were then explored through in vitro release experiments and confocal laser scanning microscopy-based analyses of the ability of these NCs to target MDA-MB-231 breast cancer cells. In addition, an MTT assay-based approach was used to compare the relative cytotoxic impact of CS/PFH-Cur-NCs and RGD-CS/PFH-Cur-NCs on these breast cancer cells. It was found that both CS/PFH-Cur-NCs and RGD-CS/PFH-Cur-NCs were smooth, relatively uniform, spheroid particles, with the latter being 531.20 ± 68.97 nm in size. These RGD-CS/PFH-Cur-NCs can be ideal for contrast imaging studies, and were better able to target breast cancer cells in comparison to CS/PFH-Cur-NCs. In addition, RGD-CS/PFH-Cur-NCs were observed to induce cytotoxic MDA-MB-231 cell death more swiftly in comparison to CS/PFH-Cur-NCs. These findings suggest that NC encapsulation and RGD surface modification can remarkably improve the anti-tumor efficacy of Cur. These novel NCs may thus manifest a significant potential value in the realm of image-guided cancer therapy, underscoring an important direction for future research.

Objective: This study explored the therapeutic impact of combined cytotoxic T lymphocyte-associated antigen 4 immunoglobulin (CTLA-4-Ig) treatment and microbubble-mediated exposure in a rat model of diabetic nephropathy (DN). Method: We treated rats using CTLA-4-Ig and/or microbubble exposure. At 8 weeks post-intervention, key parameters were evaluated including blood biochemistry, damage to renal tissue, renal parenchymal elasticity, ultrastructural changes in podocytes, and renal parenchymal expression of CD31, CD34, IL-6, Fn, Collagen I, Talin, Paxillin, α3β1, podocin, nephrin, and B7-1. Result: We found that renal function in the rat model of DN can be significantly improved by CTLA-4-Ig and CTLA-4-Ig + ultrasound microbubble treatment. Treatment efficacy was associated with reductions in renal parenchymal hardness, decreases in podocyte reduction, decreased IL-6, Fn and Collagen I expression, increased Talin, Paxillin and α3β1 expression, elevated podocin and nephrin expression, and decreased B7-1 expression. In contrast, these treatments did not impact CD31 or CD34 expression within the renal parenchyma. Conclusion: These findings clearly emphasize that CTLA-4-Ig can effectively prevent podocyte damage, inhibiting inflammation and fibrosis, and thereby treating and preventing DN. In addition, ultrasound microbubble exposure can improve the ability of CTLA-4-Ig to pass through the glomerular basement membrane in order to access podocytes such that combination CTLA-4-Ig + microbubble exposure treatment is superior to treatment with CTLA-4-Ig only.

Angiotensin II (Ang II)-induced vascular inflammation and injury entails endothelial to mesenchymal transition (EndMT). Recent studies have shown that Ang II engages toll-like receptor 4 (TLR4) in the vasculature to mediate adverse effects. Here, we aimed to investigate whether myeloid differentiation protein 2 (MD2), an extracellular molecule indispensable for TLR4 activation, mediates Ang II-induced vascular injury and EndMT. We utilized MD2 knockout mice and wildtype mice treated with a specific MD2 inhibitor to decipher its role in aortas of Ang II-challenged mice. To confirm our results and to provide mechanistic insights, we exposed cultured endothelial cells to Ang II, with or without MD2 silencing. We show that Ang II causes deleterious remodeling and EndMT in aortas of mice within two weeks. These Ang II effects were largely absent in MD2 knockout mice and in wildtype mice treated with a MD2 inhibitor. MD2 silencing in cultured endothelial cells confirmed the essential role of MD2 in Ang II-induced inflammatory factor induction, and EndMT-associated phenotypic change. We also found that Ang II-MD2-EndMT axis involves the activation of nuclear factor-κB. Our studies highlight an essential role of MD2 in Ang II-induced vascular inflammation and EndMT contributing to vascular injury. These results also imply that MD2 may be targeted to dampen inflammatory cardiovascular and EndMT-associated diseases.

Background: Hyperglycemia-associated inflammation contributes to adverse remodeling and fibrosis in diabetic heart. MyD88 is an adapter protein of many Toll-like receptors (TLRs) and is recruited to TLRs to initiate inflammatory signalling pathway in endotoxin-activated innate immunity. However, the role of MyD88 in diabetic cardiomyopathy is unknown. Methods: For genetic deficiency, cardiomyocyte-specific MyD88 knockout and littermate control mice were induced type 1 diabetes (T1D) by intraperitoneal injection of 50 mg/kg/day streptozotocin for five days consecutive and then fed for 4 moths. For pharmacological inhibition, MyD88 inhibitor LM8 were administered daily for 8 weeks by oral gavage in T1D and T2D (db/db) mice. The effect of genetic and pharmacological inhibition MyD88 to myocardial injure which were induced by 33 mM glucose in vivo. Results: In this study, we first found that MyD88 expression was increased in cardiomyocytes of diabetic mouse hearts. Cardiomyocyte-specific MyD88 knockout protected mice against hyperglycemia-induced cardiac inflammation, injury, hypertrophy, and fibrosis in T1D model. In cultured cardiomyocytes, MyD88 inhibition either by siRNA or by small-molecular inhibitor LM8 markedly blocked TLR4-MyD88 complex formation, reduced pro-inflammatory MAPKs/NF-κB cascade activation and decreased pro-inflammatory cytokine expression under high glucose condition. Moreover, pharmacologic inhibition of MyD88 by LM8 showed significantly anti-inflammatory, anti-hypertrophic and anti-fibrotic effects in the hearts of both T1D and T2D mice. These beneficial effects of MyD88 inhibition were correlated to the reduced activation of TLR4-MyD88-MAPKs/NF-κB signaling pathways in the hearts. Conclusion: Taken together, MyD88 in cardiomyocytes mediates diabetes-induced cardiac inflammatory injuries and genetic or pharmacologic inhibition of MyD88 shows significantly cardioprotective effects, indicating MyD88 as a potential therapeutic target for diabetic cardiomyopathy.