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Article ; Online: Renal Epithelial Mitochondria: Implications for Hypertensive Kidney Disease.

Stadler, Krisztian / Ilatovskaya, Daria V

Comprehensive Physiology

2023 Volume 14, Issue 1, Page(s) 5225–5242

Abstract: According to the Centers for Disease Control and Prevention, 1 in 2 U.S. adults have hypertension, and more than 1 in 7 chronic kidney disease. In fact, hypertension is the second leading cause of kidney failure in the United States; it is a complex ... ...

Abstract	According to the Centers for Disease Control and Prevention, 1 in 2 U.S. adults have hypertension, and more than 1 in 7 chronic kidney disease. In fact, hypertension is the second leading cause of kidney failure in the United States; it is a complex disease characterized by, leading to, and caused by renal dysfunction. It is well-established that hypertensive renal damage is accompanied by mitochondrial damage and oxidative stress, which are differentially regulated and manifested along the nephron due to the diverse structure and functions of renal cells. This article provides a summary of the relevant knowledge of mitochondrial bioenergetics and metabolism, focuses on renal mitochondrial function, and discusses the evidence that has been accumulated regarding the role of epithelial mitochondrial bioenergetics in the development of renal tissue dysfunction in hypertension. © 2024 American Physiological Society. Compr Physiol 14:5225-5242, 2024.
MeSH term(s)	Humans ; Kidney/metabolism ; Mitochondria/metabolism ; Hypertension ; Oxidative Stress ; Hypertension, Renal/metabolism
Language	English
Publishing date	2023-12-29
Publishing country	United States
Document type	Journal Article
ISSN	2040-4603
ISSN (online)	2040-4603
DOI	10.1002/cphy.c220033
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Article ; Online: Calcium signalling and transport in the kidney.

Staruschenko, Alexander / Alexander, R Todd / Caplan, Michael J / Ilatovskaya, Daria V

Nature reviews. Nephrology

2024

Abstract: The kidney plays a pivotal role in regulating calcium levels within the body. Approximately 98% of the filtered calcium is reabsorbed in the nephron, and this process is tightly controlled to maintain calcium homeostasis, which is required to facilitate ... ...

Abstract	The kidney plays a pivotal role in regulating calcium levels within the body. Approximately 98% of the filtered calcium is reabsorbed in the nephron, and this process is tightly controlled to maintain calcium homeostasis, which is required to facilitate optimal bone mineralization, preserve serum calcium levels within a narrow range, and support intracellular signalling mechanisms. The maintenance of these functions is attributed to a delicate balance achieved by various calcium channels, transporters, and calcium-binding proteins in renal cells. Perturbation of this balance due to deficiency or dysfunction of calcium channels and calcium-binding proteins can lead to severe complications. For example, polycystic kidney disease is linked to aberrant calcium transport and signalling. Furthermore, dysregulation of calcium levels can promote the formation of kidney stones. This Review provides an updated description of the key aspects of calcium handling in the kidney, focusing on the function of various calcium channels and the physiological stimuli that control these channels or are communicated through them. A discussion of the role of calcium as an intracellular second messenger and the pathophysiology of renal calcium dysregulation, as well as a summary of gaps in knowledge and future prospects, are also included.
Language	English
Publishing date	2024-04-19
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2490366-8
ISSN	1759-507X ; 1759-5061
ISSN (online)	1759-507X
ISSN	1759-5061
DOI	10.1038/s41581-024-00835-z
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Article ; Online: Practical notes on popular statistical tests in renal physiology.

Mamenko, Mykola / Lysikova, Daria V / Spires, Denisha R / Tarima, Sergey S / Ilatovskaya, Daria V

American journal of physiology. Renal physiology

2022 Volume 323, Issue 4, Page(s) F389–F400

Abstract: Competent statistical analysis is essential to maintain rigor and reproducibility in physiological research. Unfortunately, the benefits offered by statistics are often negated by misuse or inadequate reporting of statistical methods. To address the need ...

Abstract	Competent statistical analysis is essential to maintain rigor and reproducibility in physiological research. Unfortunately, the benefits offered by statistics are often negated by misuse or inadequate reporting of statistical methods. To address the need for improved quality of statistical analysis in papers, the
MeSH term(s)	Reproducibility of Results ; Research Design ; United States
Language	English
Publishing date	2022-07-14
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00427.2021
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Article ; Online: Transcriptomic changes in glomeruli in response to a high salt challenge in the Dahl SS rat.

Semenikhina, Marharyta / Lysikova, Daria V / Spires, Denisha R / Domondon, Mark / Stadler, Krisztian / Palygin, Oleg / Ilatovskaya, Daria V

Physiological genomics

2023 Volume 56, Issue 1, Page(s) 98–111

Abstract: Salt sensitivity impacts a significant portion of the population and is an important contributor to the development of chronic kidney disease. One of the significant early predictors of salt-induced damage is albuminuria, which reflects the deterioration ...

Abstract	Salt sensitivity impacts a significant portion of the population and is an important contributor to the development of chronic kidney disease. One of the significant early predictors of salt-induced damage is albuminuria, which reflects the deterioration of the renal filtration barrier: the glomerulus. Despite significant research efforts, there is still a gap in knowledge regarding the molecular mechanisms and signaling networks contributing to instigating and/or perpetuating salt-induced glomerular injury. To address this gap, we used 8-wk-old male Dahl salt-sensitive rats fed a normal-salt diet (0.4% NaCl) or challenged with a high-salt diet (4% NaCl) for 3 wk. At the end of the protocol, a pure fraction of renal glomeruli obtained by differential sieving was used for next-generation RNA sequencing and comprehensive semi-automatic transcriptomic data analyses, which revealed 149 differentially expressed genes (107 and 42 genes were downregulated and upregulated, respectively). Furthermore, a combination of predictive gene correlation networks and computational bioinformatic analyses revealed pathways impacted by a high salt dietary challenge, including renal metabolism, mitochondrial function, apoptotic signaling and fibrosis, cell cycle, inflammatory and immune responses, circadian clock, cytoskeletal organization, G protein-coupled receptor signaling, and calcium transport. In conclusion, we report here novel transcriptomic interactions and corresponding predicted pathways affecting glomeruli under salt-induced stress.
MeSH term(s)	Rats ; Animals ; Male ; Sodium Chloride, Dietary/adverse effects ; Sodium Chloride/metabolism ; Hypertension/genetics ; Rats, Inbred Dahl ; Blood Pressure ; Calcium/metabolism ; Transcriptome/genetics ; Gene Expression Profiling ; Kidney/metabolism
Chemical Substances	Sodium Chloride, Dietary ; Sodium Chloride (451W47IQ8X) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2023-11-13
Publishing country	United States
Document type	Journal Article
ZDB-ID	2038823-8
ISSN	1531-2267 ; 1094-8341
ISSN (online)	1531-2267
ISSN	1094-8341
DOI	10.1152/physiolgenomics.00075.2023
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Article ; Online: The implications of histamine metabolism and signaling in renal function.

Sudarikova, Anastasia V / Fomin, Mikhail V / Yankelevich, Irina A / Ilatovskaya, Daria V

Physiological reports

2021 Volume 9, Issue 8, Page(s) e14845

Abstract: Inflammation is an essential part of the immune response; it has been found to be central to the disruption of kidney function in acute kidney injury, diabetic nephropathy, hypertension, and other renal conditions. One of the well-known mediators of the ... ...

Abstract	Inflammation is an essential part of the immune response; it has been found to be central to the disruption of kidney function in acute kidney injury, diabetic nephropathy, hypertension, and other renal conditions. One of the well-known mediators of the inflammatory response is histamine. Histamine receptors are expressed throughout different tissues, including the kidney, and their inhibition has proven to be a viable strategy for the treatment of many inflammation-associated diseases. Here, we provide an overview of the current knowledge regarding the role of histamine and its metabolism in the kidney. Establishing the importance of histamine signaling for kidney function will enable new approaches for the treatment of kidney diseases associated with inflammation.
MeSH term(s)	Animals ; Histamine/metabolism ; Humans ; Kidney/metabolism ; Kidney/physiology ; Nephritis/metabolism ; Nephritis/physiopathology ; Signal Transduction
Chemical Substances	Histamine (820484N8I3)
Language	English
Publishing date	2021-04-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2724325-4
ISSN	2051-817X ; 2051-817X
ISSN (online)	2051-817X
ISSN	2051-817X
DOI	10.14814/phy2.14845
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Article: Insights Into the Molecular Mechanisms of Polycystic Kidney Diseases.

Vasileva, Valeriia Y / Sultanova, Regina F / Sudarikova, Anastasia V / Ilatovskaya, Daria V

Frontiers in physiology

2021 Volume 12, Page(s) 693130

Abstract: Autosomal dominant (AD) and autosomal recessive (AR) polycystic kidney diseases (PKD) are severe multisystem genetic disorders characterized with formation and uncontrolled growth of fluid-filled cysts in the kidney, the spread of which eventually leads ... ...

Abstract	Autosomal dominant (AD) and autosomal recessive (AR) polycystic kidney diseases (PKD) are severe multisystem genetic disorders characterized with formation and uncontrolled growth of fluid-filled cysts in the kidney, the spread of which eventually leads to the loss of renal function. Currently, there are no treatments for ARPKD, and tolvaptan is the only FDA-approved drug that alleviates the symptoms of ADPKD. However, tolvaptan has only a modest effect on disease progression, and its long-term use is associated with many side effects. Therefore, there is still a pressing need to better understand the fundamental mechanisms behind PKD development. This review highlights current knowledge about the fundamental aspects of PKD development (with a focus on ADPKD) including the PC1/PC2 pathways and cilia-associated mechanisms, major molecular cascades related to metabolism, mitochondrial bioenergetics, and systemic responses (hormonal status, levels of growth factors, immune system, and microbiome) that affect its progression. In addition, we discuss new information regarding non-pharmacological therapies, such as dietary restrictions, which can potentially alleviate PKD.
Language	English
Publishing date	2021-09-08
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2021.693130
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Article ; Online: Recent advances in understanding ion transport mechanisms in polycystic kidney disease.

Sudarikova, Anastasia V / Vasileva, Valeriia Y / Sultanova, Regina F / Ilatovskaya, Daria V

Clinical science (London, England : 1979)

2021 Volume 135, Issue 21, Page(s) 2521–2540

Abstract: This review focuses on the most recent advances in the understanding of the electrolyte transport-related mechanisms important for the development of severe inherited renal disorders, autosomal dominant (AD) and recessive (AR) forms of polycystic kidney ... ...

Abstract	This review focuses on the most recent advances in the understanding of the electrolyte transport-related mechanisms important for the development of severe inherited renal disorders, autosomal dominant (AD) and recessive (AR) forms of polycystic kidney disease (PKD). We provide here a basic overview of the origins and clinical aspects of ARPKD and ADPKD and discuss the implications of electrolyte transport in cystogenesis. Special attention is devoted to intracellular calcium handling by the cystic cells, with a focus on polycystins and fibrocystin, as well as other calcium level regulators, such as transient receptor potential vanilloid type 4 (TRPV4) channels, ciliary machinery, and purinergic receptor remodeling. Sodium transport is reviewed with a focus on the epithelial sodium channel (ENaC), and the role of chloride-dependent fluid secretion in cystic fluid accumulation is discussed. In addition, we highlight the emerging promising concepts in the field, such as potassium transport, and suggest some new avenues for research related to electrolyte handling.
MeSH term(s)	Animals ; Humans ; Ion Transport ; Kidney/metabolism ; Kidney/physiopathology ; Membrane Transport Proteins/genetics ; Membrane Transport Proteins/metabolism ; Mutation ; Polycystic Kidney, Autosomal Dominant/genetics ; Polycystic Kidney, Autosomal Dominant/metabolism ; Polycystic Kidney, Autosomal Dominant/physiopathology ; Polycystic Kidney, Autosomal Recessive/genetics ; Polycystic Kidney, Autosomal Recessive/metabolism ; Polycystic Kidney, Autosomal Recessive/physiopathology ; Receptors, Cell Surface/genetics ; Receptors, Cell Surface/metabolism ; TRPP Cation Channels/genetics ; TRPP Cation Channels/metabolism ; Water-Electrolyte Balance
Chemical Substances	Membrane Transport Proteins ; PKHD1 protein, human ; Receptors, Cell Surface ; TRPP Cation Channels ; polycystic kidney disease 1 protein ; polycystic kidney disease 2 protein
Language	English
Publishing date	2021-11-09
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	206835-7
ISSN	1470-8736 ; 0301-0538 ; 0009-0360 ; 0143-5221
ISSN (online)	1470-8736
ISSN	0301-0538 ; 0009-0360 ; 0143-5221
DOI	10.1042/CS20210370
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Article ; Online: Probenecid slows disease progression in a murine model of autosomal dominant polycystic kidney disease.

Arkhipov, Sergey N / Potter, D'Anna L / Sultanova, Regina F / Ilatovskaya, Daria V / Harris, Peter C / Pavlov, Tengis S

Physiological reports

2023 Volume 11, Issue 7, Page(s) e15652

Abstract: Development of autosomal dominant polycystic kidney disease (ADPKD) involves renal epithelial cell abnormalities. Cystic fluid contains a high level of ATP that, among other effects, leads to a reduced reabsorption of electrolytes in cyst-lining cells, ... ...

Abstract	Development of autosomal dominant polycystic kidney disease (ADPKD) involves renal epithelial cell abnormalities. Cystic fluid contains a high level of ATP that, among other effects, leads to a reduced reabsorption of electrolytes in cyst-lining cells, and thus results in cystic fluid accumulation. Earlier, we demonstrated that Pkd1
MeSH term(s)	Mice ; Male ; Female ; Humans ; Animals ; Polycystic Kidney, Autosomal Dominant/drug therapy ; Polycystic Kidney, Autosomal Dominant/genetics ; Polycystic Kidney, Autosomal Dominant/metabolism ; Probenecid/pharmacology ; Probenecid/metabolism ; Probenecid/therapeutic use ; Disease Models, Animal ; Kidney/metabolism ; Disease Progression ; Adenosine Triphosphate/metabolism ; Cysts/metabolism ; Cysts/pathology ; TRPP Cation Channels/genetics ; TRPP Cation Channels/metabolism ; TRPP Cation Channels/pharmacology
Chemical Substances	Probenecid (PO572Z7917) ; Adenosine Triphosphate (8L70Q75FXE) ; TRPP Cation Channels
Language	English
Publishing date	2023-04-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2724325-4
ISSN	2051-817X ; 2051-817X
ISSN (online)	2051-817X
ISSN	2051-817X
DOI	10.14814/phy2.15652
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Article ; Online: Nitric-Oxide-Mediated Signaling in Podocyte Pathophysiology.

Semenikhina, Marharyta / Stefanenko, Mariia / Spires, Denisha R / Ilatovskaya, Daria V / Palygin, Oleg

Biomolecules

2022 Volume 12, Issue 6

Abstract: Nitric oxide (NO) is a potent signaling molecule involved in many physiological and pathophysiological processes in the kidney. NO plays a complex role in glomerular ultrafiltration, vasodilation, and inflammation. Changes in NO bioavailability in ... ...

Abstract	Nitric oxide (NO) is a potent signaling molecule involved in many physiological and pathophysiological processes in the kidney. NO plays a complex role in glomerular ultrafiltration, vasodilation, and inflammation. Changes in NO bioavailability in pathophysiological conditions such as hypertension or diabetes may lead to podocyte damage, proteinuria, and rapid development of chronic kidney disease (CKD). Despite the extensive data highlighting essential functions of NO in health and pathology, related signaling in glomerular cells, particularly podocytes, is understudied. Several reports indicate that NO bioavailability in glomerular cells is decreased during the development of renal pathology, while restoring NO level can be beneficial for glomerular function. At the same time, the compromised activity of nitric oxide synthase (NOS) may provoke the formation of peroxynitrite and has been linked to autoimmune diseases such as systemic lupus erythematosus. It is known that the changes in the distribution of NO sources due to shifts in NOS subunits expression or modifications of NADPH oxidases activity may be linked to or promote the development of pathology. However, there is a lack of information about the detailed mechanisms describing the production and release of NO in the glomerular cells. The interaction of NO and other reactive oxygen species in podocytes and how NO-calcium crosstalk regulates glomerular cells' function is still largely unknown. Here, we discuss recent reports describing signaling, synthesis, and known pathophysiological mechanisms mediated by the changes in NO homeostasis in the podocyte. The understanding and further investigation of these essential mechanisms in glomerular cells will facilitate the design of novel strategies to prevent or manage health conditions that cause glomerular and kidney damage.
MeSH term(s)	Humans ; Kidney/metabolism ; Kidney Glomerulus/metabolism ; Kidney Glomerulus/pathology ; Nitric Oxide ; Nitric Oxide Synthase/metabolism ; Podocytes/metabolism ; Podocytes/pathology ; Proteinuria/metabolism
Chemical Substances	Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase (EC 1.14.13.39)
Language	English
Publishing date	2022-05-25
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom12060745
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Article: Editorial: Role of Molecular Modulators in Combatting Cardiac Injury and Disease: Prevention, Repair and Regeneration.

de Castro Brás, Lisandra E / Schibalski, Ryan S / Ilatovskaya, Daria V / O'Meara, Caitlin C / DeLeon-Pennell, Kristine Y

Frontiers in cardiovascular medicine

2022 Volume 9, Page(s) 861442

Language	English
Publishing date	2022-04-18
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2781496-8
ISSN	2297-055X
ISSN	2297-055X
DOI	10.3389/fcvm.2022.861442
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