Journal of Yeungnam Medical Science

Review articles

Comprehensive overview of the role of mitochondrial dysfunction in the pathogenesis of acute kidney ischemia-reperfusion injury: a narrative review: Min-Ji Kim, Chang Joo Oh, Chang-Won Hong, Jae-Han Jeon; J Yeungnam Med Sci. 2024;41(2):61-73. Published online February 14, 2024; DOI: https://doi.org/10.12701/jyms.2023.01347

858 View
54 Download

Abstract PDF: Acute kidney ischemia-reperfusion (IR) injury is a life-threatening condition that predisposes individuals to chronic kidney disease. Since the kidney is one of the most energy-demanding organs in the human body and mitochondria are the powerhouse of cells, mitochondrial dysfunction plays a central role in the pathogenesis of IR-induced acute kidney injury. Mitochondrial dysfunction causes a reduction in adenosine triphosphate production, loss of mitochondrial dynamics (represented by persistent fragmentation), and impaired mitophagy. Furthermore, the pathological accumulation of succinate resulting from fumarate reduction under oxygen deprivation (ischemia) in the reverse flux of the Krebs cycle can eventually lead to a burst of reactive oxygen species driven by reverse electron transfer during the reperfusion phase. Accumulating evidence indicates that improving mitochondrial function, biogenesis, and dynamics, and normalizing metabolic reprogramming within the mitochondria have the potential to preserve kidney function during IR injury and prevent progression to chronic kidney disease. In this review, we summarize recent advances in understanding the detrimental role of metabolic reprogramming and mitochondrial dysfunction in IR injury and explore potential therapeutic strategies for treating kidney IR injury.

Can antioxidants be effective therapeutics for type 2 diabetes?: Soyoung Park, So-Young Park; Yeungnam Univ J Med. 2021;38(2):83-94. Published online October 8, 2020; DOI: https://doi.org/10.12701/yujm.2020.00563

10,158 View
212 Download
10 Crossref

The global obesity epidemic and the growing elderly population largely contribute to the increasing incidence of type 2 diabetes. Insulin resistance acts as a critical link between the present obesity pandemic and type 2 diabetes. Naturally occurring reactive oxygen species (ROS) regulate intracellular signaling and are kept in balance by the antioxidant system. However, the imbalance between ROS production and antioxidant capacity causes ROS accumulation and induces oxidative stress. Oxidative stress interrupts insulin-mediated intracellular signaling pathways, as supported by studies involving genetic modification of antioxidant enzymes in experimental rodents. In addition, a close association between oxidative stress and insulin resistance has been reported in numerous human studies. However, the controversial results with the use of antioxidants in type 2 diabetes raise the question of whether oxidative stress plays a critical role in insulin resistance. In this review article, we discuss the relevance of oxidative stress to insulin resistance based on genetically modified animal models and human trials.

Citations

Citations to this article as recorded by

Effect of substitution of wheat flour with chickpea flour on their physico-chemical characteristics
Jiwan S. Sidhu, Tasleem Zafar, Abdulwahab Almusallam, Muslim Ali, Amani Al-Othman
Arab Gulf Journal of Scientific Research.2023;[Epub] CrossRef
The consumption of date palm fruits as a source of bioactive compounds in patients with type 2 diabetes: a cross sectional study
M.Q. Al-Mssallem
Acta Horticulturae.2023; (1371): 381. CrossRef
Aging, oxidative stress and degenerative diseases: mechanisms, complications and emerging therapeutic strategies
Mani Raj Chaudhary, Sakshi Chaudhary, Yogita Sharma, Thokchom Arjun Singh, Alok Kumar Mishra, Shweta Sharma, Mohammad Murtaza Mehdi
Biogerontology.2023; 24(5): 609. CrossRef
Development and Characterization of Oxidatively Responsive Thiol–Ene Networks for Bone Graft Applications
Tyler Touchet, Samuel Briggs, Lance Graul, Duncan J. Maitland
ACS Applied Bio Materials.2022; 5(6): 2633. CrossRef
Prevalence of Sarcopenia and Its Association With Diabetes: A Meta-Analysis of Community-Dwelling Asian Population
Seung Min Chung, Jun Sung Moon, Min Cheol Chang
Frontiers in Medicine.2021;[Epub] CrossRef
Association of Prx4, Total Oxidant Status, and Inflammatory Factors with Insulin Resistance in Polycystic Ovary Syndrome
Sahar Mazloomi, Nasrin Sheikh, Marzieh Sanoee Farimani, Shamim Pilehvari, Raffaele Pezzani
International Journal of Endocrinology.2021; 2021: 1. CrossRef
Plants Secondary Metabolites as Blood Glucose-Lowering Molecules
Mayadah Bashir Shehadeh, Ghadeer A. R. Y. Suaifan, Ala’ Mustafa Abu-Odeh
Molecules.2021; 26(14): 4333. CrossRef
An Epidemiological Study Report on the Antioxidant and Phenolic Content of Selected Mediterranean Functional Foods, Their Consumption Association with the Body Mass Index, and Consumers Purchasing Behavior in a Sample of Healthy Greek Adults
Aikaterini Kandyliari, Ioannis-Nektarios Elmaliklis, Olga Kontopoulou, Marianna Tsafkopoulou, Georgios Komninos, Christina Ntzatha, Andreas Petsas, Haralabos C. Karantonis, Antonios E. Koutelidakis
Applied Sciences.2021; 11(17): 7818. CrossRef
Sterculia tragacantha Lindl Leaf Extract Ameliorates STZ-Induced Diabetes, Oxidative Stress, Inflammation and Neuronal Impairment
Amos Sunday Onikanni, Bashir Lawal, Augustine O Olusola, Janet O Olugbodi, Saidu Sani, Basiru Olaitan Ajiboye, Omotayo B Ilesanmi, Mohammed Alqarni, Gomaa Mostafa-Hedeab, Ahmad J Obaidullah, Gaber El-Saber Batiha, Alexander TH Wu
Journal of Inflammation Research.2021; Volume 14: 6749. CrossRef
Methionine sulfoxide reductase B3 deficiency inhibits the development of diet-induced insulin resistance in mice
Hye-Na Cha, Chang-Hoon Woo, Hwa-Young Kim, So-Young Park
Redox Biology.2020; : 101823. CrossRef

Reviews

Novel non-apoptotic cell death: ferroptosis: Seon Min Woo, Taeg Kyu Kwon; Yeungnam Univ J Med. 2017;34(2):174-181. Published online December 31, 2017; DOI: https://doi.org/10.12701/yujm.2017.34.2.174

2,099 View
31 Download

Abstract PDF: Ferroptosis is a newly recognized type of cell death that results from iron-dependent lipid peroxidation and is different from other types of cell death, such as apoptosis, necrosis, and autophagic cell death. This type of cell death is characterized by mitochondrial shrinkage with an increased mitochondrial membrane density and outer mitochondrial membrane rupture. Ferroptosis can be induced by a loss of activity of system Xc− and the inhibition of glutathione peroxidase 4, followed by the accumulation of lipid reactive oxygen species (ROS). In addition, inactivation of the mevalonate and transsulfuration pathways is involved in the induction of ferroptosis. Moreover, nicotinamide adenine dinucleotide phosphate oxidase and p53 promote ferroptosis by increasing ROS production, while heat shock protein beta-1 and nuclear factor erythroid 2-related factor 2 inhibit ferroptosis by reducing iron uptake. This article outlines the molecular mechanisms and signaling pathways of ferroptosis regulation, and explains the roles of ferroptosis in human disease.

The relationship between muscle mitochondrial nutritional overloading and insulin resistance: Jae Han Jeon, Jun Sung Moon, Kyu Chang Won, In Kyu Lee; Yeungnam Univ J Med. 2017;34(1):19-28. Published online June 30, 2017; DOI: https://doi.org/10.12701/yujm.2017.34.1.19

1,900 View
20 Download

Abstract PDF: The incidence of type 2 diabetes mellitus and insulin resistance is growing rapidly. Multiple organs including the liver, skeletal muscle and adipose tissue control insulin sensitivity coordinately, but the mechanism of skeletal muscle insulin resistance has not yet been fully elucidated. However, there is a growing body of evidence that lipotoxicity induced by mitochondrial dysfunction in skeletal muscle is an important mediator of insulin resistance. However, some recent findings suggest that skeletal mitochondrial dysfunction generated by genetic manipulation is not always correlated with insulin resistance in animal models. A high fat diet can provoke insulin resistance despite a coordinate increase in skeletal muscle mitochondria, which implies that mitochondrial dysfunction is not mandatory in insulin resistance. Furthermore, incomplete fatty acid oxidation by excessive nutrition supply compared to mitochondrial demand can induce insulin resistance without preceding impairment of mitochondrial function. Taken together we suggested that skeletal muscle mitochondrial overloading, not mitochondrial dysfunction, plays a pivotal role in insulin resistance.

Original Article

Role of Extracellular Signal-Regulated Kinase 1/2 and Reactive Oxygen Species in Toll-Like Receptor 2-Mediated Dual-Specificity Phosphatase 4 Expression.: So Yeon Kim, Suk Hwan Baek; Yeungnam Univ J Med. 2013;30(1):10-16. Published online June 30, 2013; DOI: https://doi.org/10.12701/yujm.2013.30.1.10

1,923 View
8 Download

Abstract PDF: BACKGROUND
Toll-like receptors (TLRs) are well-known pattern recognition receptors. Among the 13 TLRs, TLR2 is the most known receptor for immune response. It activates mitogen-activated protein kinases (MAPKs), which are counterbalanced by MAPK phosphatases [MKPs or dual-specificity phosphatases (DUSPs)]. However, the regulatory mechanism of DUSPs is still unclear. In this study, the effect of a TLR2 ligand (TLR2L, Pam3CSK4) on DUSP4 expression in Raw264.7 cells was demonstrated. METHODS: A Raw264.7 mouse macrophage cell line was cultured in Dulbecco's modified Eagle's medium supplemented with 10% fetal bovine serum and 1% antibiotics (100 U/mL penicillin and 100 g/mL streptomycin) at 37degrees C in 5% CO2. TLR2L (Pam3CSK4)-mediated DUSP4 expressions were confirmed with RT-PCR and western blot analysis. In addition, the detection of reactive oxygen species (ROS) was measured with lucigenin assay. RESULTS: Pam3CSK4 induced the expression of DUSP1, 2, 4, 5 and 16. The DUSP4 expression was also increased by TLR4 and 9 agonists (lipopolysaccharide and CpG ODN, respectively). Pam3CSK4 also induced ERK1/2 phosphorylation and ROS production, and the Pam3CSK4-induced DUSP4 expression was decreased by ERK1/2 (U0126) and ROS (DPI) inhibitors. U0126 suppressed the ROS production by Pam3CSK4. CONCLUSION: Pam3CSK4-mediated DUSP4 expression is regulated by ERK1/2 and ROS. This finding suggests the physiological importance of DUSP4 in TLR2-mediated immune response.

First
Prev
Page of 1
Next
Last

Search