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Pathobiology of Acute Kidney Injury 2.0
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Pathobiology of Acute Kidney Injury 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (15 November 2022) | Viewed by 9384

Special Issue Editors

Dr. Amandeep Bajwa

E-Mail Website1 Website2
Guest Editor
Transplant Research Institute, James D. Eason Transplant Institute, Department of Surgery, School of Medicine, University of Tennessee Health Science Center, Memphis, TN, USA
Interests: reperfusion Injury; kidney; mitochondria; acute kidney injury
Special Issues, Collections and Topics in MDPI journals
Dr. Navjot Pabla

E-Mail Website
Guest Editor
Comprehensive Cancer Center & School of Pharmacy Ohio State University, Columbus, OH 43210, USA
Interests: Kidney Diseases; acute kidney injury; renal cell carcinoma
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Acute kidney injury (AKI) is a common clinical condition associated with diverse etiologies and abrupt loss of renal function. In patients with sepsis, rhabdomyolysis, cancer, as well as cardiovascular disorders, the underlying disease or associated therapeutic interventions can cause hypoxic, cytotoxic, and inflammatory insults to renal parenchymal cells (endothelial and epithelial) resulting in the onset of AKI. Furthermore, the pathogenesis of kidney injury following AKI involves a complex interaction between altered microcirculatory hemodynamics, renal parenchymal cells and infiltrating innate and adaptive immune cells. Considerable data support that the immune system mediates AKI, yet many of the underlying mechanisms still remain unclear. Furthermore, lack of clinical data, supporting the involvement of the immune system in AKI pathogenesis, has hindered the development of clinically tenable anti-inflammatory options. Therefore, dialysis presently remains the only treatment option available to AKI patients, underscoring the need to develop novel approaches to tackle this hurdle to ultimately improve patient quality of life. Thus, in order to better understand these complexities of AKI, it is necessary to clarify these interplays. In this Special Issue on “Pathobiology of Acute Kidney Injury”, we will discuss various mediators of inflammation to further understand their interactions that result in AKI.

Dr. Amandeep Bajwa
Dr. Navjot Pabla
Guest Editors

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Keywords

  • acute kidney injury
  • inflammation
  • tubular epithelial cells
  • immune cells
  • macrophages
  • neutrophils
  • innate immunity
  • adaptive immunity
  • mitochondria
  • apoptosis
  • necrosis

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Published Papers (4 papers)

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Research

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15 pages, 2701 KiB  
Article
Partial Genetic Deletion of Klotho Aggravates Cardiac Calcium Mishandling in Acute Kidney Injury
by Laura González-Lafuente, José Alberto Navarro-García, Ángela Valero-Almazán, Elena Rodríguez-Sánchez, Sara Vázquez-Sánchez, Elisa Mercado-García, Patricia Pineros, Jonay Poveda, María Fernández-Velasco, Makoto Kuro-O, Luis M. Ruilope and Gema Ruiz-Hurtado
Int. J. Mol. Sci. 2023, 24(2), 1322; https://doi.org/10.3390/ijms24021322 - 10 Jan 2023
Cited by 2 | Viewed by 2338
Abstract
Acute kidney injury (AKI) is associated with an elevated risk of cardiovascular major events and mortality. The pathophysiological mechanisms underlying the complex cardiorenal network interaction remain unresolved. It is known that the presence of AKI and its evolution are significantly associated with an [...] Read more.
Acute kidney injury (AKI) is associated with an elevated risk of cardiovascular major events and mortality. The pathophysiological mechanisms underlying the complex cardiorenal network interaction remain unresolved. It is known that the presence of AKI and its evolution are significantly associated with an alteration in the anti-aging factor klotho expression. However, it is unknown whether a klotho deficiency might aggravate cardiac damage after AKI. We examined intracellular calcium (Ca2+) handling in native ventricular isolated cardiomyocytes from wild-type (+/+) and heterozygous hypomorphic mice for the klotho gene (+/kl) in which an overdose of folic acid was administered to induce AKI. Twenty-four hours after AKI induction, cardiomyocyte contraction was decreased in mice with the partial deletion of klotho expression (heterozygous hypomorphic klotho named +/kl). This was accompanied by alterations in Ca2+ transients during systole and an impairment of sarco/endoplasmic reticulum Ca2+-ATPase (SERCA2a) function in +/kl mice after AKI induction. Moreover, Ca2+ spark frequency and the incidence of Ca2+ pro-arrhythmic events were greater in cardiomyocytes from heterozygous hypomorphic klotho compared to wild-type mice after AKI. A decrease in klotho expression plays a role in cardiorenal damage aggravating cardiac Ca2+ mishandling after an AKI, providing the basis for future targeted approaches directed to control klotho expression as novel therapeutic strategies to reduce the cardiac burden that affects AKI patients. Full article
(This article belongs to the Special Issue Pathobiology of Acute Kidney Injury 2.0)
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17 pages, 4583 KiB  
Article
Histone Deacetylases Cooperate with NF-κB to Support the Immediate Migratory Response after Zebrafish Pronephros Injury
by Mingyue Zhuang, Alexander Scholz, Gerd Walz and Toma Antonov Yakulov
Int. J. Mol. Sci. 2022, 23(17), 9582; https://doi.org/10.3390/ijms23179582 - 24 Aug 2022
Cited by 2 | Viewed by 2059
Abstract
Acute kidney injury (AKI) is commonly associated with severe human diseases, and often worsens the outcome in hospitalized patients. The mammalian kidney has the ability to recover spontaneously from AKI; however, little progress has been made in the development of supportive treatments. Increasing [...] Read more.
Acute kidney injury (AKI) is commonly associated with severe human diseases, and often worsens the outcome in hospitalized patients. The mammalian kidney has the ability to recover spontaneously from AKI; however, little progress has been made in the development of supportive treatments. Increasing evidence suggest that histone deacetylases (HDAC) and NF-κB promote the pathogenesis of AKI, and inhibition of Hdac activity has a protective effect in murine models of AKI. However, the role of HDAC at the early stages of recovery is unknown. We used the zebrafish pronephros model to study the role of epigenetic modifiers in the immediate repair response after injury to the tubular epithelium. Using specific inhibitors, we found that the histone deacetylase Hdac2, Hdac6, and Hdac8 activities are required for the repair via collective cell migration. We found that hdac6, hdac8, and nfkbiaa expression levels were upregulated in the repairing epithelial cells shortly after injury. Depletion of hdac6, hdac8, or nfkbiaa with morpholino oligonucleotides impaired the repair process, whereas the combined depletion of all three genes synergistically suppressed the recovery process. Furthermore, time-lapse video microscopy revealed that the lamellipodia and filopodia formation in the flanking cells was strongly reduced in hdac6-depleted embryos. Our findings suggest that Hdac activity and NF-κB are synergistically required for the immediate repair response in the zebrafish pronephros model of AKI, and the timing of HDAC inhibition might be important in developing supportive protocols in the human disease. Full article
(This article belongs to the Special Issue Pathobiology of Acute Kidney Injury 2.0)
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13 pages, 2780 KiB  
Article
Slc25a39 and Slc25a40 Expression in Mice with Bile Duct Ligation or Lipopolysaccharide Treatment
by Atsushi Kawase, Momoko Hatanaka, Naoya Matsuda, Hiroaki Shimada and Masahiro Iwaki
Int. J. Mol. Sci. 2022, 23(15), 8573; https://doi.org/10.3390/ijms23158573 - 2 Aug 2022
Cited by 2 | Viewed by 2178
Abstract
SLC25A39/40, involved in mitochondrial GSH (mGSH) import from the cytoplasm, is essential for protection against oxidative stress and mitochondrial dysfunction. We examined the effects of cholestasis, through bile duct ligation (BDL) and lipopolysaccharide (LPS)-induced inflammation in mice, on Slc25a39/40 expression. Additionally, we used [...] Read more.
SLC25A39/40, involved in mitochondrial GSH (mGSH) import from the cytoplasm, is essential for protection against oxidative stress and mitochondrial dysfunction. We examined the effects of cholestasis, through bile duct ligation (BDL) and lipopolysaccharide (LPS)-induced inflammation in mice, on Slc25a39/40 expression. Additionally, we used human clear cell renal carcinoma (KMRC-1) cells to elucidate the mechanism of regulation of SLC25A39/40 expression in the kidneys after LPS treatment. BDL resulted in a decrease in Slc25a39 mRNA in the liver and a decrease in Slc25a39/40 mRNA and protein in the kidneys. Consequently, there was a significant decrease in mGSH levels in the kidneys of BDL mice compared with those in sham mice. LPS treatment resulted in increased Slc25a40 expression in the kidneys. In KMRC-1 cells, the combination treatment of LPS-RS or FPS-ZM1 with LPS suppressed the LPS-induced increase in SLC25A40, suggesting that SLC25A40 expression could be regulated by the signaling pathway via toll-like receptor 4 and the receptor for advanced glycation end products, respectively. Our findings contribute to understanding the role of mGSH in the maintenance of the mitochondrial redox state. To the best of our knowledge, this is the first study that demonstrates the changes in Slc25a39/40 expression in mice with cholestasis-associated renal injury and LPS-induced inflammation. Full article
(This article belongs to the Special Issue Pathobiology of Acute Kidney Injury 2.0)
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Review

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13 pages, 626 KiB  
Review
Update on Innate Immunity in Acute Kidney Injury—Lessons Taken from COVID-19
by Kinga Musiał
Int. J. Mol. Sci. 2022, 23(20), 12514; https://doi.org/10.3390/ijms232012514 - 19 Oct 2022
Cited by 2 | Viewed by 2171
Abstract
The serious clinical course of SARS-CoV-2 infection is usually accompanied by acute kidney injury (AKI), worsening prognosis and increasing mortality. AKI in COVID-19 is above all a consequence of systemic dysregulations leading to inflammation, thrombosis, vascular endothelial damage and necrosis. All these processes [...] Read more.
The serious clinical course of SARS-CoV-2 infection is usually accompanied by acute kidney injury (AKI), worsening prognosis and increasing mortality. AKI in COVID-19 is above all a consequence of systemic dysregulations leading to inflammation, thrombosis, vascular endothelial damage and necrosis. All these processes rely on the interactions between innate immunity elements, including circulating blood cells, resident renal cells, their cytokine products, complement systems, coagulation cascades and contact systems. Numerous simultaneous pathways of innate immunity should secure an effective host defense. Since they all form a network of cross-linked auto-amplification loops, uncontrolled activation is possible. When the actions of selected pathways amplify, cascade activation evades control and the propagation of inflammation and necrosis worsens, accompanied by complement overactivity and immunothrombosis. The systemic activation of innate immunity reaches the kidney, where the damage affecting single tubular cells spreads through tissue collateral damage and triggers AKI. This review is an attempt to synthetize the connections between innate immunity components engaged in COVID-19-related AKI and to summarize the knowledge on the pathophysiological background of processes responsible for renal damage. Full article
(This article belongs to the Special Issue Pathobiology of Acute Kidney Injury 2.0)
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