Article
Biochemistry & Molecular Biology
Yasuaki Sawashita, Satoshi Kazuma, Yasuyuki Tokinaga, Kenichiro Kikuchi, Naoyuki Hirata, Yoshiki Masuda, Michiaki Yamakage
Summary: This study showed that albumin administration prevents the shedding of endothelial glycocalyx (GCX) in myocardial ischemia-reperfusion (I/R) injury via the S1P receptor. Additionally, the S1P receptor agonist fingolimod attenuates the protective effect of albumin by downregulating the receptor.
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
(2023)
Article
Medical Laboratory Technology
Makoto Kurano, Kazuhisa Tsukamoto, Tomo Shimizu, Masumi Hara, Yutaka Yatomi
Summary: Diabetic nephropathy is a common cause of end-stage renal failure and associated mortality worldwide. The ApoM/S1P axis plays a role in the pathogenesis/progression of diabetic nephropathy. Higher ApoM levels are associated with a lower clinical stage of diabetic nephropathy. In a mouse model, deletion of ApoM worsens the phenotypes of diabetic nephropathy while overexpression of ApoM ameliorates them.
TRANSLATIONAL RESEARCH
(2023)
Article
Biotechnology & Applied Microbiology
Hanying Ding, Jinxiang Li, Yang Li, Minliang Yang, Sheng Nie, Miaomiao Zhou, Zhanmei Zhou, Xiaobing Yang, Youhua Liu, Fan Fan Hou
Summary: This study identified miR-10a/b as negative regulators of NLRP3 inflammasome in diabetic kidney disease, preventing renal inflammation and reducing albuminuria. Targeting miR-10a/b could be a novel intervention strategy for inhibiting kidney inflammation in DKD.
Article
Medicine, General & Internal
Fangfei Zhang, Jianyong Yin, Li Liu, Shuiying Liu, Guangyuan Zhang, Yiwei Kong, Yajun Wang, Niansong Wang, Xiangmei Chen, Feng Wang
Summary: In this study, the researchers investigated the therapeutic effects of IL-17C blockade on AKI and DN. They found that delayed IL-17C neutralization can protect against renal ischemia-reperfusion injury and attenuate DN in mice. They also discovered that IL-17C expression is increased in patients with DN and IL-17C blockade can reduce albuminuria, mesangial matrix accumulation, and podocyte loss in DN.
Review
Biochemistry & Molecular Biology
Jessica M. Overstreet, Cody C. Gifford, Jiaqi Tang, Paul J. Higgins, Rohan Samarakoon
Summary: p53 is widely known for its role in tumorigenesis, but recent studies have found its involvement in the initiation and progression of various renal diseases. The activation and elevated expression of p53 are associated with conditions such as ischemia, aristolochic acid (AA) exposure, diabetes, HIV infection, obstruction, and podocyte-induced nephropathies. Research using mouse models has confirmed the pathogenic role of p53 in acute kidney injury and chronic kidney disease through chemical or renal-specific inhibition. Understanding the mechanisms of p53 in renal diseases is important for developing therapeutic strategies.
CELLULAR AND MOLECULAR LIFE SCIENCES
(2022)
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
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
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
Beata Roka, Pal Tod, Tamas Kaucsar, Eva Nora Bukosza, Imre Voros, Zoltan V. Varga, Balazs Petrovich, Bence Agg, Peter Ferdinandy, Gabor Szenasi, Peter Hamar
Summary: Delayed contralateral nephrectomy improved kidney function after IR and decreased fibrosis progression. miRNAs play a crucial role in this process.
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)
Review
Medicine, Research & Experimental
Fatemeh Sabet Sarvestani, Negar Azarpira, Ismail H. Al-Abdullah, Ali-Mohammad Tamaddon
Summary: Ischemia reperfusion injury can lead to tissue damage, especially during organ transplantation. By manipulating miRNAs level, they can be used as a biomarker for early diagnosis of IRI or suggestive to be therapeutic agents in clinical situation in future.
BIOMEDICINE & PHARMACOTHERAPY
(2021)
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
Multidisciplinary Sciences
Dou Huang, Changwei Chen, Yunxia Zuo, Lei Du, Ting Liu, Geoffrey W. Abbott, Zhaoyang Hu
Summary: This study found that RLIPost reduces pulmonary damage induced by ischemia-reperfusion in both non-diabetic and diabetic rats. The protective mechanism in non-diabetic rats is associated with STAT-3, while in diabetic rats it is independent of STAT-3.
Article
Urology & Nephrology
Keisuke Sako, Kengo Furuichi, Shohei Makiishi, Yuta Yamamura, Toshiya Okumura, Hong Thu Le, Shinji Kitajima, Tadashi Toyama, Akinori Hara, Yasunori Iwata, Norihiko Sakai, Miho Shimizu, Fumio Niimura, Taiji Matsusaka, Shuichi Kaneko, Takashi Wada
Summary: Paired box 2 (Pax2) is an essential transcription factor for kidney development and is reactivated during recovery from kidney injury. This study reveals that Pax2 reactivation plays a role in the regulation of cell proliferation in proximal tubular epithelial cells (PTECs). Knockout of Pax2 leads to increased interstitial fibrosis, decreased cell proliferation, and increased apoptotic cells.
KIDNEY INTERNATIONAL
(2022)
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)
