The Role of Cardiolipin and Mitochondrial Damage in Kidney Transplant

Miranda-Díaz, Alejandra Guillermina; Cardona-Muñoz, Ernesto Germán; Pacheco-Moisés, Fermín Paul

doi:10.1155/2019/3836186

Cited by 18 publications

(17 citation statements)

References 132 publications

(147 reference statements)

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“…The surface area of the IMM is more than four times larger than that of the OMM [ 16 ]. Shortage in cardiolipin results in decreases in length and number of cristae, and in the overall surface area of IMM, which, in turn, reduces the ATP production [ 17 ].…”

Section: Cardiolipin and Mitochondrial Bioenergeticsmentioning

confidence: 99%

Cardiolipin, Non-Bilayer Structures and Mitochondrial Bioenergetics: Relevance to Cardiovascular Disease

Gasanoff

Yaguzhinsky

Garab

2021

Cells

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The present review is an attempt to conceptualize a contemporary understanding about the roles that cardiolipin, a mitochondrial specific conical phospholipid, and non-bilayer structures, predominantly found in the inner mitochondrial membrane (IMM), play in mitochondrial bioenergetics. This review outlines the link between changes in mitochondrial cardiolipin concentration and changes in mitochondrial bioenergetics, including changes in the IMM curvature and surface area, cristae density and architecture, efficiency of electron transport chain (ETC), interaction of ETC proteins, oligomerization of respiratory complexes, and mitochondrial ATP production. A relationship between cardiolipin decline in IMM and mitochondrial dysfunction leading to various diseases, including cardiovascular diseases, is thoroughly presented. Particular attention is paid to the targeting of cardiolipin by Szeto–Schiller tetrapeptides, which leads to rejuvenation of important mitochondrial activities in dysfunctional and aging mitochondria. The role of cardiolipin in triggering non-bilayer structures and the functional roles of non-bilayer structures in energy-converting membranes are reviewed. The latest studies on non-bilayer structures induced by cobra venom peptides are examined in model and mitochondrial membranes, including studies on how non-bilayer structures modulate mitochondrial activities. A mechanism by which non-bilayer compartments are formed in the apex of cristae and by which non-bilayer compartments facilitate ATP synthase dimerization and ATP production is also presented.

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Section: Cardiolipin and Mitochondrial Bioenergeticsmentioning

confidence: 99%

Cardiolipin, Non-Bilayer Structures and Mitochondrial Bioenergetics: Relevance to Cardiovascular Disease

Gasanoff

Yaguzhinsky

Garab

2021

Cells

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“…Studies have found that cardiolipin, located in the mitochondrial intima, is prone to peroxidation. Cardiolipin oxidation is necessary to promote the release of apoptotic factors in the process of mitochondriadriven apoptosis [24]. These studies have shown that lipid peroxidation of membrane phospholipids has a wide range of effects through changes in membrane structure and function, as well as through protein-lipid interactions.…”

Section: Discussionmentioning

confidence: 99%

Aquaporin 9 Represents a Novel Target of Chronic Liver Injury That May Antagonize Its Progression by Reducing Lipotoxicity

Cheng

Ding

Fang

et al. 2021

Oxidative Medicine and Cellular Longevity

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In recent years, chronic liver injury has become a common disease that harms human health. Its clinical manifestations are hepatic steatosis and secondary chronic steatohepatitis, which can quickly transform into liver fibrosis and cirrhosis if not treated in time. Therefore, this study is aimed at searching for new therapeutic targets of chronic liver injury and clarifying the molecular mechanisms of the new targets involved in chronic liver injury. After aquaporin 9 was identified as a target by proteomics, Aqp9-/- mice were constructed using the CRISPR/Cas9 system. Biochemical and morphological tests were used to verify the effect of Aqp9 knockout on early chronic liver injury. Proteomics, molecular biology, and morphology experiments were used to screen and verify the effects of Aqp9 knockout on its downstream pathway. Through the above experiments, we demonstrated that aquaporin 9 could be used as an intervention target for antagonizing the development of early chronic liver injury and its gene knockout affected downstream inflammation, oxidative stress, apoptosis, and pyroptosis by alleviating hepatic lipotoxicity.

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“…Cardiolipin, an inner mitochondrial membrane phospholipid that facilitates electron transfer by cristae modulation, has been studied as a candidate target [43]. Elamipretide (SS-31), which selectively binds cardiolipin and inhibits cardiolipin peroxidation during oxidative stress [44], was shown to have renocardioprotective properties [45,46] and to improve skeletal muscle mitochondrial energetics [47][48][49] in animal models.…”

Section: Therapeutic Approachesmentioning

confidence: 99%

Skeletal muscle energetics in patients with moderate to advanced kidney disease

Ertuğlu

Yıldız

Gamboa

et al. 2022

Kidney Res Clin Pract

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Sarcopenia, defined as decrease in muscle function and mass, is common in patients with moderate to advanced chronic kidney disease (CKD) and is associated with poor clinical outcomes. Muscle mitochondrial dysfunction is proposed as one of the mechanisms underlying sarcopenia. Patients with moderate to advanced CKD have decreased muscle mitochondrial content and oxidative capacity along with suppressed activity of various mitochondrial enzymes such as mitochondrial electron transport chain complexes and pyruvate dehydrogenase, leading to impaired energy production. Other mitochondrial abnormalities found in this population include defective beta-oxidation of fatty acids and mitochondrial DNA mutations. These changes are noticeable from the early stages of CKD and correlate with severity of the disease. Damage induced by uremic toxins, oxidative stress, and systemic inflammation has been implicated in the development of mitochondrial dysfunction in CKD patients. Given that mitochondrial function is an important determinant of physical activity and performance, its modulation is a potential therapeutic target for sarcopenia in patients with kidney disease. Coenzyme Q, nicotinamide, and cardiolipin-targeted peptides have been tested as therapeutic interventions in early studies. Aerobic exercise, a well-established strategy to improve muscle function and mass in healthy adults, is not as effective in patients with advanced kidney disease. This might be due to reduced expression or impaired activation of peroxisome proliferator-activated receptor-gamma coactivator 1α, the master regulator of mitochondrial biogenesis. Further studies are needed to broaden our understanding of the pathogenesis of mitochondrial dysfunction and to develop mitochondrial-targeted therapies for prevention and treatment of sarcopenia in patients with CKD.

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The Role of Cardiolipin and Mitochondrial Damage in Kidney Transplant

Cited by 18 publications

References 132 publications

Cardiolipin, Non-Bilayer Structures and Mitochondrial Bioenergetics: Relevance to Cardiovascular Disease

Cardiolipin, Non-Bilayer Structures and Mitochondrial Bioenergetics: Relevance to Cardiovascular Disease

Aquaporin 9 Represents a Novel Target of Chronic Liver Injury That May Antagonize Its Progression by Reducing Lipotoxicity

Skeletal muscle energetics in patients with moderate to advanced kidney disease

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