Article
Urology & Nephrology
Jennifer S. Y. Li, Harry Robertson, Katie Trinh, Arti M. Raghubar, Quan Nguyen, Nicholas Matigian, Ellis Patrick, Angus W. Thomson, Andrew J. Mallett, Natasha M. Rogers
Summary: Ischemia reperfusion injury is a common cause of acute kidney injury. Adoptively transferred tolerogenic dendritic cells can successfully limit kidney injury and provide protection against ischemia reperfusion injury.
KIDNEY INTERNATIONAL
(2023)
Article
Biochemistry & Molecular Biology
Heng-Chih Pan, Yau-Hung Chen, Wei-Ching Fang, Vin-Cent Wu, Chiao-Yin Sun
Summary: KDM4C plays a critical role in kidney development and acute kidney injury (AKI). Knockdown of KDM4C leads to impaired kidney development and decreased cell survival in zebrafish and mouse models. Furthermore, KDM4C may exert a protective effect on cell survival in AKI by regulating mitochondrial dynamics and function.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Biochemistry & Molecular Biology
Benedikt Kolbrink, Friedrich Alexander von Samson-Himmelstjerna, Maja Lucia Messtorff, Theresa Riebeling, Raphael Nische, Jessica Schmitz, Jan Hinrich Brasen, Ulrich Kunzendorf, Stefan Krautwald
Summary: Ferroptosis, a type of iron-dependent programmed cell death, plays a vital role in multiple diseases. However, there are no pharmacologic inhibitors of ferroptosis in clinical use. In this study, vitamin K1 was identified as an efficient inhibitor of ferroptosis, providing a new strategy for pharmacological control of this mode of cell death.
CELLULAR AND MOLECULAR LIFE SCIENCES
(2022)
Article
Engineering, Biomedical
Weimin Tang, Sudipta Panja, Chinmay M. Jogdeo, Siyuan Tang, Ling Ding, Ao Yu, Kirk W. Foster, Del L. Dsouza, Yashpal S. Chhonker, Heather Jensen-Smith, Hee-Seong Jang, Erika I. Boesen, Daryl J. Murry, Babu Padanilam, David Oupicky
Summary: This study demonstrates the synthesis of a novel siRNA carrier, C-CS, which shows potential for targeted delivery to injured kidneys. The C-CS/siRNA nanoparticles effectively accumulate and deliver therapeutic siRNAs to injured kidneys through CXCR4 binding, providing a new approach for AKI therapy.
Article
Cell Biology
Izumi Nagayama, Kaori Takayanagi, Hajime Hasegawa, Akito Maeshima
Summary: In this study, the expression and localization of follistatin in normal and ischemic rat kidneys were examined, and urinary follistatin levels were measured to assess its potential as a biomarker for acute kidney injury. The results showed that follistatin was mainly localized in the distal tubules of the cortex in normal kidneys, while it was also present in the distal tubules of both the cortex and outer medulla in ischemic kidneys. Urinary follistatin levels were significantly increased in ischemic rats and correlated with the duration of ischemia, the follistatin-positive area, and the acute tubular damage area.
Article
Biochemistry & Molecular Biology
Johanna Stoermer, Wilfried Gwinner, Katja Derlin, Stephan Immenschuh, Song Rong, Mi-Sun Jang, Nelli Shushakova, Hermann Haller, Faikah Gueler, Robert Greite
Summary: This study investigated the effects of diclofenac on the progression of AKI and long-term renal consequences in the setting of pre-existing subclinical AKI. The results showed that diclofenac aggravated renal injury in a dose and time-dependent manner and even a single dose can cause progression to chronic kidney disease.
Article
Immunology
Jiefu Zhu, Yafei Zhang, Lang Shi, Yao Xia, Hongchu Zha, Huimin Li, Zhixia Song
Summary: This study reveals the protective role of RP105 in ischemic and septic acute kidney injury (AKI). Overexpression of RP105 alleviated renal structural injuries and dysfunction caused by ischemic and septic AKI. RP105 suppressed inflammatory responses mediated by the TLR4 signaling pathway. These findings suggest that RP105 could be a potential target for preventing and treating ischemic and septic AKI.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2022)
Article
Immunology
Lijuan Ma, Xueqi Liu, Mengya Zhang, Lang Zhou, Ling Jiang, Li Gao, Xian Wang, Yuebo Huang, Hanxu Zeng, Yonggui Wu
Summary: This article discusses the complicated pathophysiological mechanism of acute kidney injury (AKI) and the lack of effective drugs. It also introduces a newly discovered cell death mode called ferroptosis, which is involved in the progression of AKI. Paeoniflorin (PF), a traditional Chinese medicine, has protective effects on kidney diseases including AKI, but the mechanism of PF in attenuating AKI is unclear.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2023)
Article
Oncology
Kyungho Lee, Hye Ryoun Jang, Junseok Jeon, Kyeong Eun Yang, Jung Eun Lee, Ghee Young Kwon, Dae Joong Kim, Yoon-Goo Kim, Wooseong Huh
Summary: The repair mechanism after ischemic acute kidney injury (AKI) involves complex immunologic processes that determine long-term renal outcomes. By investigating two murine ischemia-reperfusion injury (IRI) models, it was found that the immune changes and inflammatory conditions in the post-ischemic kidneys are related to the recovery of renal function, and the bilateral IRI model differs from the unilateral IRI model in terms of immune response and inflammation severity.
AMERICAN JOURNAL OF TRANSLATIONAL RESEARCH
(2022)
Article
Biochemistry & Molecular Biology
Chih-Chao Yang, Pei-Hsun Sung, John Y. Chiang, Han-Tan Chai, Chih-Hung Chen, Yi-Ching Chu, Yi-Chen Li, Hon-Kan Yip
Summary: Combined tacrolimus and melatonin therapy was more effective than either single treatment in protecting the kidney from IR injury by suppressing inflammation and oxidative stress.
Article
Nanoscience & Nanotechnology
Chenguang Ding, Bo Wang, Jin Zheng, Mingzhen Zhang, Yang Li, Hsin-Hui Shen, Yingcong Guo, Bingxuan Zheng, Puxun Tian, Xiaoming Ding, Wujun Xue
Summary: Ischemia/reperfusion (I/R) injury leads to excessive oxidative events and destructive inflammatory responses, playing a key role in various pathological conditions. Ferroptosis, a type of iron-dependent nonapoptotic cell death, is associated with I/R injury diseases. Excessive production of inflammatory cytokines contributes to the development of acute kidney injury. In this study, neutrophil membrane-coated copper-based nanoparticles (N-Cu5.4O@DFO NPs) demonstrated excellent antioxidant and iron ion scavenging abilities, effectively reducing oxidative damage and inflammatory response in the kidney, presenting a potential therapeutic strategy for renal I/R injury. This work also promotes the development of nanoantioxidant agents for the treatment of other I/R injury diseases.
ACS APPLIED MATERIALS & INTERFACES
(2023)
Article
Pharmacology & Pharmacy
Jiajia Li, Yupeng Jiang, Qin Dai, Yue Yu, Xin Lv, Yan Zhang, Xiaohua Liao, Liyun Ao, Gaoyun Hu, Jie Meng, Zhangzhe Peng, Lijian Tao, Yanyun Xie
Summary: In this study, the protective effect of Mefunidone on ischemia-reperfusion injury-induced acute kidney injury was investigated. The results showed that Mefunidone can protect the kidney by relieving kidney tubular injury, suppressing oxidative stress, and inhibiting cell apoptosis. Furthermore, Mefunidone reduced mitochondrial damage and protected mitochondrial function.
FRONTIERS IN PHARMACOLOGY
(2022)
Article
Chemistry, Physical
Xishao Xie, Yunjing Zhang, Xinwan Su, Junni Wang, Xi Yao, Dou Lv, Qin Zhou, Jianhua Mao, Jianghua Chen, Fei Han, Yangyang Li, Weiqiang Lin
Summary: This study synthesized gallic acid-gallium polyvinyl pyrrolidone nanoparticles (GGP NPs) as a potential iron-scavenging agent and demonstrated their good biocompatibility and protective effects in inhibiting ferroptosis. Treatment with GGP NPs significantly ameliorated renal injury and mitochondrial damage, making them a potential candidate for AKI treatment.
Article
Pharmacology & Pharmacy
Zengying Liu, Chen Guan, Chenyu Li, Ningxin Zhang, Chengyu Yang, Lingyu Xu, Bin Zhou, Long Zhao, Hong Luan, Xiaofei Man, Yan Xu
Summary: This study found that tilianin has a protective effect on I/R-induced AKI through the ERK/EGR1/BCL2L1 pathway by using bioinformatics analysis. It provides new insights into the protective effect and underlying molecular mechanisms of tilianin on I/R-induced AKI.
FRONTIERS IN PHARMACOLOGY
(2022)
Article
Chemistry, Multidisciplinary
Qian Chen, Fei Ding, Shuangye Zhang, Qian Li, Xiaoguo Liu, Haiyun Song, Xiaolei Zuo, Chunhai Fan, Shan Mou, Zhilei Ge
Summary: The development of a renal-accumulating DNA nanodevice in this study offers promising protection for acute kidney injury patients in different stages, with potential for providing durable and pathogenic treatment for kidney dysfunction based on the pathophysiological events caused by ischemia-reperfusion.
Article
Urology & Nephrology
Jiefu Zhu, Gang Zhang, Zhixia Song, Xiaohong Xiang, Shaoqun Shu, Zhiwen Liu, Danyi Yang, Qingqing Wei, Zheng Dong
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
(2020)
Editorial Material
Urology & Nephrology
Qingqing Wei
KIDNEY INTERNATIONAL
(2020)
Review
Oncology
Siyao Li, Lu Wen, Xiaoru Hu, Qingqing Wei, Zheng Dong
Summary: Cisplatin, a commonly used chemotherapy drug, is limited by its nephrotoxicity, but hypoxia-inducible factor (HIF) activation may protect against kidney injury during cisplatin chemotherapy. While HIF activation has been shown to have beneficial effects in experimental models of acute kidney injury caused by cisplatin, more research is needed on its effects in chronic kidney problems following cisplatin treatment. Prolyl hydroxylase (PHD) inhibitors, which induce HIF, may offer promise in protecting kidneys during cisplatin chemotherapy, but their potential impact on the anti-cancer effects of cisplatin needs further investigation.
Article
Urology & Nephrology
Sarah R. McLarnon, Katie Wilson, Bansari Patel, Jingping Sun, Christina L. Sartain, Christopher D. Mejias, Jacqueline B. Musall, Jennifer C. Sullivan, Qingqing Wei, Jian-Kang Chen, Kelly A. Hyndman, Brendan Marshall, Haichun Yang, Agnes B. Fogo, Paul M. O'Connor
Summary: This study reveals the origin of vascular congestion in the renal medulla and its association with early tubular injury. Furthermore, by manipulating renal medullary blood flow during reperfusion, it is possible to prevent vascular congestion and its associated tubular injury.
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
(2022)
Article
Cell Biology
Shuangshuang Fu, Xiaoru Hu, Zhengwei Ma, Qingqing Wei, Xiaohong Xiang, Siyao Li, Lu Wen, Yumei Liang, Zheng Dong
Summary: The protein p53 in proximal tubular cells plays an important role in the development of chronic kidney problems following cisplatin chemotherapy.
Review
Medicine, General & Internal
Lu Wen, Ying Li, Siyao Li, Xiaoru Hu, Qingqing Wei, Zheng Dong
Summary: The kidneys play a crucial role in glucose homeostasis and abnormal glucose metabolism is associated with kidney diseases such as acute kidney injury. This review discusses the regulation of glucose homeostasis in kidneys and the impact of glucose metabolism on different types of AKI. Further research on glucose metabolism in kidney injury and repair could lead to the discovery of new therapeutic targets for kidney diseases.
FRONTIERS IN MEDICINE
(2021)
Article
Medicine, Research & Experimental
Riyaz Mohamed, Gene R. Crislip, Sarah McLarnon, Qingqing Wei, Paul M. O'Connor, Jennifer C. Sullivan
Summary: Acute kidney injury (AKI) due to ischemia is a serious complication with high mortality rates. Vascular congestion following ischemia-reperfusion (IR) injury has been linked to worsened outcomes. This study found that male spontaneously hypertensive rats (SHR) had greater vascular congestion and impaired renal recovery following renal IR compared to female SHR and normotensive male Sprague-Dawley rats (SD). Preventing increases in blood pressure did not alter sustained vascular congestion. These findings highlight the importance of vascular congestion on impaired renal recovery.
Article
Biochemistry & Molecular Biology
Shuqin Mei, Lin Li, Xiangjun Zhou, Cheng Xue, Man J. Livingston, Qingqing Wei, Bing Dai, Zhiguo Mao, Changlin Mei, Zheng Dong
Summary: Diabetes enhances kidney fibrosis by enhancing HIF-1 activation, leading to impaired kidney repair. In diabetic mice, unilateral ureteral obstruction induces more renal fibrosis, apoptosis, and interstitial macrophage infiltration. High glucose-conditioned renal tubular cells show higher expression of fibrosis marker protein under hypoxia, which is mediated by increased HIF-1α expression. Knockout of proximal tubule-specific HIF-1α attenuates fibrosis induced by UUO in diabetic mice kidneys.
Article
Medical Laboratory Technology
Lu Wen, Qingqing Wei, Man J. Livingston, Guie Dong, Siyao Li, Xiaoru Hu, Ying Li, Yuqing Huo, Zheng Dong
Summary: This study reveals the induction of PFKFB3 in cisplatin nephrotoxicity and its novel role in activating the CDK4/Rb pathway. Inhibition or silencing of PFKFB3 reduces cisplatin-induced apoptosis in renal cells and ameliorates kidney injury in mice. Blocking PFKFB3 presents a potential kidney protective strategy for cancer patients undergoing cisplatin therapy.
TRANSLATIONAL RESEARCH
(2023)
Article
Cell Biology
Qiuhua Yang, Emily Huo, Yongfeng Cai, Zhidan Zhang, Charles Dong, John M. Asara, Qingqing Wei
Summary: This study demonstrates the critical role of glycolytic activator PFKFB3 in driving fibroblast activation and subsequent renal fibrosis. It also highlights the promoting effect of lactate on renal fibrosis.
Article
Immunology
Qiuhua Yang, Emily Huo, Yongfeng Cai, Zhidan Zhang, Charles Dong, John M. Asara, Huidong Shi, Qingqing Wei
Summary: Excessive renal fibrosis is a common pathology in progressive chronic kidney diseases. In this study, the researchers found that glycolytic pathway genes are upregulated in renal myeloid cells during kidney fibrosis. By inhibiting the glycolytic activator Pfkfb3, they observed reduced fibrosis, decreased macrophage infiltration, and alterations in macrophage subtypes and phenotypes. Mechanistically, they found that glycolytic metabolites stabilize HIF1α, leading to changes in macrophage phenotypes that contribute to renal fibrosis.
FRONTIERS IN IMMUNOLOGY
(2023)
Article
Immunology
Indumathi Manoharan, Daniel Swafford, Arulkumaran Shanmugam, Nikhil Patel, Puttur D. Prasad, Riyaz Mohamed, Qingqing Wei, Zheng Dong, Muthusamy Thangaraju, Santhakumar Manicassamy
Summary: This study reveals the critical role of the Wnt-LRP5/6 signaling pathway in macrophages in regulating colitis-induced systemic inflammation and acute kidney injury (AKI). Conditional deletion of LRP5/6 in macrophages enhances susceptibility to colitis-induced systemic inflammation and AKI in mice. Aggravated colitis-associated systemic inflammation and AKI in LRP5/6-deficient mice are attributed to increased bacterial translocation and elevated proinflammatory cytokine levels in the kidney. Furthermore, macrophages lacking LRP5/6 produce higher levels of proinflammatory cytokines due to hyperresponsiveness to TLR ligands and increased activation of MAPKs.
JOURNAL OF IMMUNOLOGY
(2022)
Article
Physiology
G. Ryan Crislip, Bansari Patel, Riyaz Mohamed, Sarah C. Ray, Qingqing Wei, Jingping Sun, Aaron J. Polichnowski, Jennifer C. Sullivan, Paul M. O'Connor
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
(2020)
Article
Physiology
Zhixia Song, Jiefu Zhu, Qingqing Wei, Guie Dong, Zheng Dong
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
(2020)
Article
Physiology
Qingqing Wei, Jennifer Su, Guie Dong, Ming Zhang, Yuqing Huo, Zheng Dong
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
(2019)