Article
Critical Care Medicine
Haibing Sun, Huiping Jiang, Amity Eliaz, John A. Kellum, Zhiyong Peng, Isaac Eliaz
Summary: Gal-3 plays a crucial role in the pathogenesis of S-AKI and its inhibitor P-MCP shows potential as a therapeutic target, significantly reducing mortality and incidence of severe sepsis-associated AKI.
Article
Immunology
Maomao Sun, Jiaxin Li, Liangfeng Mao, Jie Wu, Zhiya Deng, Man He, Sheng An, Zhenhua Zeng, Qiaobing Huang, Zhongqing Chen
Summary: Recent studies have shown that upregulation of autophagy can attenuate sepsis-induced acute kidney injury (SAKI). The tumor suppressor protein p53 has been identified as a regulator of autophagy in various forms of acute kidney injury. Acetylation of p53 exacerbates AKI, but deacetylation can promote RTEC autophagy and alleviate SAKI.
FRONTIERS IN IMMUNOLOGY
(2021)
Review
Immunology
Shankun Zhao, Jian Liao, Maolei Shen, Xin Li, Mei Wu
Summary: Sepsis-induced acute kidney injury (SI-AKI) is a leading cause of global death, and autophagy has been identified as a key modulator in SI-AKI. This review summarizes the proposed roles of autophagy in SI-AKI, revealing that autophagy levels are often elevated during the progression of SI-AKI. Various signaling molecules and pathways are involved in the process of SI-AKI, affecting autophagy and subsequently impacting kidney function. Targeting autophagy-associated proteins and pathways may offer new treatment prospects for critically ill patients with SI-AKI, although further preclinical studies are needed to validate this hypothesis.
FRONTIERS IN IMMUNOLOGY
(2023)
Review
Medicine, General & Internal
Zhifen Wu, Junhui Deng, Hongwen Zhou, Wei Tan, Lirong Lin, Jurong Yang
Summary: Sepsis-associated acute kidney injury (SA-AKI) is commonly seen in ICU patients with severe sepsis and has a high mortality rate. Most patients develop AKI before drug treatment. Research has shown that the main mechanism of SA-AKI is vasodilation, hypotension, and shock leading to inadequate renal blood perfusion, resulting in ischemia and necrosis of renal tubular cells. Various forms of programmed cell death, including apoptosis, necroptosis, pyroptosis, and autophagy, play important roles in SA-AKI.
FRONTIERS IN MEDICINE
(2022)
Article
Cell Biology
Zhiya Deng, Maomao Sun, Jie Wu, Haihong Fang, Shumin Cai, Sheng An, Qiaobing Huang, Zhenfeng Chen, Chenglun Wu, Ziwei Zhou, Haoran Hu, Zhenhua Zeng
Summary: The study demonstrates that activation of SIRT1 can promote autophagy and attenuate sepsis-induced acute kidney injury (SAKI). SIRT1 only deacetylates Beclin1, mediating autophagy and protection against SAKI through deacetylation of Beclin1 at K430 and K437. This suggests that pharmacologic induction of autophagy via SIRT1-mediated Beclin1 deacetylation may be a promising therapeutic approach for future SAKI treatment.
CELL DEATH & DISEASE
(2021)
Article
Agriculture, Multidisciplinary
Qibin Wu, Zhenxiang Li, Jingtao Yang, Fu Xu, Xueqin Fu, Liping Xu, Chuihuai You, Dongjiao Wang, Yachun Su, Youxiong Que
Summary: This study reports the first comprehensive analysis of protein lysine acetylation, 2-hydroxyisobutyrylation, and lysine lactylation in sugarcane. These post-translational modifications were found to be involved in energy metabolism and stress response. The results provide new insights into the molecular mechanisms of protein PTMs in sugarcane.
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
(2023)
Review
Biochemistry & Molecular Biology
Michael Takla, Swati Keshri, David C. Rubinsztein
Summary: TFEB is a critical transcription factor involved in multiple physiological functions. Pathological states modify TFEB function by regulating its post-translational modifications, which can have both protective and deleterious effects on tissue survival. Understanding the post-translational modifications of TFEB is important for the development of diseases such as neurodegeneration and cancer.
Review
Medicine, Research & Experimental
Jian-Chun Li, Lin-Jun Wang, Fei Feng, Ting-Ting Chen, Wen-Gui Shi, Li-Ping Liu
Summary: Sepsis-related acute kidney injury (S-AKI) is a common and significant complication of sepsis in critically ill patients, which can often only be treated with antibiotics and medications that reduce S-AKI symptoms. The precise mechanism underlying the onset of S-AKI is still unclear, thus hindering the development of new strategies for its treatment. Therefore, it is necessary to explore the pathogenesis of S-AKI to identify biomarkers and therapeutic targets for its early diagnosis and treatment. Heparanase (HPA), the only known enzyme that cleaves the side chain of heparan sulfate, has been widely studied in relation to tumor metabolism, procoagulant activity, angiogenesis, inflammation and sepsis. It has been reported that HPA plays an important role in the progression of S-AKI. The aim of the present review was to provide an overview of the function of HPA in S-AKI and to summarize its underlying molecular mechanisms, including mediating inflammatory response, immune response, autophagy and exosome biogenesis. It is anticipated that emerging discoveries about HPA in S-AKI will support HPA as a potential biomarker and therapeutic target to combat S-AKI.
EXPERIMENTAL AND THERAPEUTIC MEDICINE
(2023)
Review
Biochemistry & Molecular Biology
Yu-Ming Chang, Yu-Ting Chou, Wei-Chih Kan, Chih-Chung Shiao
Summary: This review discusses the bidirectional interplay and pathophysiological mechanisms between sepsis and acute kidney injury (AKI), as well as preventive strategies for these conditions. The primary pathophysiology of sepsis-associated AKI involves inflammation, vascular dysfunction, cell cycle arrest, and apoptosis. On the other hand, the pathophysiology of sepsis following AKI includes fluid overload, hyperinflammation, immunosuppression, and infection associated with kidney replacement therapy and catheter cannulation. Several limitations persistently prevent a full understanding of the bidirectional pathophysiologies.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Review
Pharmacology & Pharmacy
Fang-Fang He, Yu-Mei Wang, Yi-Yuan Chen, Wei Huang, Zi-Qi Li, Chun Zhang
Summary: Sepsis is a complex clinical syndrome caused by infectious or noninfectious factors. Acute kidney injury (AKI) is a common and severe complication of sepsis, and recent evidence suggests that autophagy and natural products may have therapeutic effects on sepsis-associated AKI.
FRONTIERS IN PHARMACOLOGY
(2022)
Article
Pharmacology & Pharmacy
Zhang Qiongyue, Yang Xin, Peng Meng, Mi Sulin, Wang Yanlin, Li Xinyi, Song Xuemin
Summary: This study demonstrates the involvement of ferroptosis, a new type of cell death, in the pathogenesis of sepsis-associated acute kidney injury (SA-AKI). The results show that post-treatment with irisin can inhibit ferroptosis and alleviate SA-AKI through the activation of the SIRT1/Nrf2 signaling pathway.
FRONTIERS IN PHARMACOLOGY
(2022)
Article
Oncology
Zhenzhen Sang, Shimin Dong, Pu Zhang, Yunxia Wei
Summary: The study demonstrated that miR-214 alleviated AKI in septic mice by inhibiting kidney autophagy levels. miR-214 further inhibited autophagy by silencing PTEN expression in the kidney tissues of septic mice. These results suggest that miR-214 ameliorated CLP-induced AKI by reducing oxidative stress and inhibiting autophagy through the regulation of the PTEN/AKT/mTOR pathway.
MOLECULAR MEDICINE REPORTS
(2021)
Review
Physiology
Rongsong Li, Yang Xiao, Kang Li, Ling Tian
Summary: This review summarizes the recent research on autophagy regulated at both transcriptional and post-translational levels by insect hormone in cooperation with other signals, such as nutrient, in insects, providing a reference and deeper understanding for studying autophagy in insects.
FRONTIERS IN PHYSIOLOGY
(2022)
Review
Plant Sciences
William Agbemafle, Min May Wong, Diane C. Bassham
Summary: This review summarizes key regulatory mechanisms for modulating autophagy through post-translational modification or transcriptional regulation. Plants activate cellular responses to adapt to changing environmental conditions, one of which is autophagy, where cellular components are delivered to the vacuole for degradation. Autophagy is activated by various conditions, and the pathways controlling its activation are being elucidated. However, there is still much to discover regarding how these factors work together to properly modulate autophagy in response to specific signals.
JOURNAL OF EXPERIMENTAL BOTANY
(2023)
Article
Biochemistry & Molecular Biology
Karlie R. Platz, Emma J. Rudisel, Katelynn V. Paluch, Taylor R. Laurin, Kristin E. Dittenhafer-Reed
Summary: The mitochondrial proteome undergoes various post-translational modifications, and this study focused on the effects of acetylation and phosphorylation on the function of mitochondrial RNA polymerase (POLRMT). While some modifications showed slight decrease in the binding ability of POLRMT, there were minimal biological impacts observed in terms of viability, mtDNA content, and mitochondrial transcript levels.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
