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Article: Association of New-Onset Atrial Fibrillation With All-Cause Mortality in COVID-19 Patients.

Zaheer, Kamran / Goncalves, Bruno / Ramalingam, Archana / Rabbani, Noor Ul Ann / Sayyed, Rameez / Nawab, Athar / Puri, Raghav / Williams, Charles J / Mansoor, Kanaan

Cureus

2023 Volume 15, Issue 12, Page(s) e49785

Abstract: Background The COVID-19 pandemic has brought about unprecedented global health challenges, with its impact extending beyond respiratory manifestations to encompass cardiovascular complications, including arrhythmias. Dysrhythmias in COVID-19 are ... ...

Abstract	Background The COVID-19 pandemic has brought about unprecedented global health challenges, with its impact extending beyond respiratory manifestations to encompass cardiovascular complications, including arrhythmias. Dysrhythmias in COVID-19 are multifactorial, ranging from direct myocardial insult due to the cytokine storm to metabolic derangements. Objective In this study, we aim to examine the incidence of new-onset atrial fibrillation and to study its association with all-cause mortality of COVID-19. Methods A cross-sectional study was conducted at Cabell Huntington Hospital, West Virginia, utilizing electronic medical records of COVID-19 patients from 2020 to 2021. Inclusion criteria comprised patients aged >18 years with COVID-19 diagnosis and cardiac arrhythmias during hospitalization. Logistic regression analysis was employed to examine the relationship between demographic and clinical variables and in-hospital mortality. Results Of the 264 eligible patients, those aged >66 years had lower odds of in-hospital mortality (p < 0.001), while gender, ejection fraction, and diabetes mellitus did not significantly predict mortality. Atrial fibrillation (p = 0.011) and heart failure (p = 0.030) were associated with increased odds of mortality, while hypertension showed no significant predictive power (p = 0.791). Conclusion This study highlights the significance of atrial fibrillation and heart failure as predictors of in-hospital mortality in COVID-19 patients. Our findings underscore the importance of recognizing and managing arrhythmias in COVID-19 and call for further research on the mechanisms and long-term effects of these cardiac complications in the context of the pandemic. These insights can guide clinical practice and interventions to optimize patient outcomes.
Language	English
Publishing date	2023-12-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	2747273-5
ISSN	2168-8184
ISSN	2168-8184
DOI	10.7759/cureus.49785
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Inhibition of Na/K-ATPase signaling Attenuates Steatohepatitis and Atherosclerosis in Mice Fed a Western Diet.

Sodhi, Komal / Srikanthan, Krithika / Goguet-Rubio, Perrine / Nichols, Alexandra / Nawab, Athar / Shah, Preeya / Chaudhry, Muhammad / El-Hamdani, Mehiar / Xie, Zijian / Shapiro, Joseph

Cellular and molecular biology (Noisy-le-Grand, France)

2023 Volume 69, Issue 2, Page(s) 162–171

Abstract: We have previously reported that the α1 subunit of sodium-potassium adenosine triphosphatase (Na/K-ATPase), acts as a receptor and an amplifier for reactive oxygen species, in addition to its distinct pumping function. On this background, we speculated ... ...

Abstract	We have previously reported that the α1 subunit of sodium-potassium adenosine triphosphatase (Na/K-ATPase), acts as a receptor and an amplifier for reactive oxygen species, in addition to its distinct pumping function. On this background, we speculated that the blockade of Na/K-ATPase-induced ROS amplification with a specific peptide, pNaKtide, might attenuate the development of steatohepatitis. To test this hypothesis, pNaKtide was administered to a murine model of NASH: the C57Bl6 mouse fed a "western" diet containing high amounts of fat and fructose. The administration of pNaKtide reduced obesity as well as hepatic steatosis, inflammation and fibrosis. Of interest, we also noted a marked improvement in mitochondrial fatty acid oxidation, insulin sensitivity, dyslipidemia and aortic streaking in this mouse model. To further elucidate the effects of pNaKtide on atherosclerosis, similar studies were performed in ApoE knockout mice also exposed to the western diet. In these mice, pNaKtide not only improved steatohepatitis, dyslipidemia, and insulin sensitivity but also ameliorated significant aortic atherosclerosis. Collectively, this study demonstrates that the Na/K-ATPase/ROS amplification loop contributes significantly to the development and progression of steatohepatitis and atherosclerosis. Furthermore, this study presents a potential treatment, the pNaKtide, for the metabolic syndrome phenotype.
MeSH term(s)	Animals ; Mice ; Diet, Western/adverse effects ; Insulin Resistance ; Reactive Oxygen Species ; Atherosclerosis/drug therapy ; Fatty Liver/drug therapy ; Mice, Inbred C57BL ; Adenosine Triphosphatases
Chemical Substances	Reactive Oxygen Species ; Adenosine Triphosphatases (EC 3.6.1.-)
Language	English
Publishing date	2023-02-28
Publishing country	France
Document type	Journal Article
ZDB-ID	1161779-2
ISSN	1165-158X ; 0145-5680
ISSN (online)	1165-158X
ISSN	0145-5680
DOI	10.14715/cmb/2023.69.2.27
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Article ; Online: Adipocyte Na, K-ATPase Signaling Attenuates Experimental Uremic Cardiomyopathy.

Sodhi, Komal / Wang, Xiaoliang / Chaudhary, Muhammad A / Lakhani, Hari Vishal / Zehra, Mishghan / Nawab, Athar / Cottrill, Cameron L / Bai, Fang / Liu, Jiang / Sanabria, Juan R / Xie, Zijian / Shapiro, Joseph I

Cellular and molecular biology (Noisy-le-Grand, France)

2023 Volume 69, Issue 5, Page(s) 197–206

Abstract: Oxidative stress has been shown to cause an alteration of intracellular signaling in adipocytes that may lead to various comorbidities of obesity and cardiovascular complications. Evidence suggests that dysregulation of Na, K-ATPase signaling can ... ...

Abstract	Oxidative stress has been shown to cause an alteration of intracellular signaling in adipocytes that may lead to various comorbidities of obesity and cardiovascular complications. Evidence suggests that dysregulation of Na, K-ATPase signaling can contribute to systemic inflammation and redox signaling that leads to various metabolic disturbances. Hence the present study aims to explore the specific role of adipocyte Na, K-ATPase signaling in the amelioration of pathophysiological alterations of experimental uremic cardiomyopathy. Experimental uremic cardiomyopathy was induced by partial nephrectomy (PNx), and adipocyte-specific expression of NaKtide, a peptide that inhibits Na, K-ATPase signaling, was achieved using a lentivirus construct with NaKtide expression driven by an adiponectin promoter. Cardiomyopathy and anemia induced in partial nephrectomy mice were accompanied by an altered molecular phenotype of adipocytes, increased systemic inflammatory cytokines and oxidant stress within 4 weeks. These changes were significantly worsened by the addition of a Western diet (enriched in fat and fructose contents) but were prevented with specific expression of NaKtide in adipocytes. The skeletal muscle-specific expression of NaKtide did not ameliorate the disease phenotype. Adipocyte dysfunction and uremic cardiomyopathy developed in PNx mice, both were significantly ameliorated by the adipocyte-specific expression of NaKtide. These findings suggest that oxidative milieu in the adipocyte has a pivotal role in the development and progression of uremic cardiomyopathy in mice subjected to partial nephrectomy. If confirmed in humans, this may be a lead for future research to explore novel therapeutic targets in chronic renal failure.
MeSH term(s)	Humans ; Mice ; Animals ; Cardiomyopathies/etiology ; Cardiomyopathies/metabolism ; Sodium-Potassium-Exchanging ATPase/metabolism ; Signal Transduction ; Oxidative Stress ; Peptides/metabolism ; Adipocytes/metabolism
Chemical Substances	Sodium-Potassium-Exchanging ATPase (EC 7.2.2.13) ; Peptides
Language	English
Publishing date	2023-05-31
Publishing country	France
Document type	Journal Article
ZDB-ID	1161779-2
ISSN	1165-158X ; 0145-5680
ISSN (online)	1165-158X
ISSN	0145-5680
DOI	10.14715/cmb/2023.69.5.31
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Article ; Online: Retraction Note: The Adipocyte Na/K-ATPase Oxidant Amplification Loop is the Central Regulator of Western Diet-Induced Obesity and Associated Comorbidities.

Pratt, Rebecca D / Brickman, Cameron / Nawab, Athar / Cottrill, Cameron / Snoad, Brian / Lakhani, Hari Vishal / Jelcick, Austin / Henderson, Brandon / Bhardwaj, Niharika N / Sanabria, Juan R / Liu, Jiang / Xie, Zijian / Abraham, Nader G / Shapiro, Joseph I / Sodhi, Komal

Scientific reports

2022 Volume 12, Issue 1, Page(s) 9005

Language	English
Publishing date	2022-05-30
Publishing country	England
Document type	Journal Article ; Retraction of Publication
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-13459-9
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Article ; Online: Retraction Note: pNaKtide Attenuates Steatohepatitis and Atherosclerosis by Blocking Na/K-ATPase/ROS Amplification in C57Bl6 and ApoE Knockout Mice Fed a Western Diet.

Sodhi, Komal / Srikanthan, Krithika / Goguet-Rubio, Perrine / Nichols, Alexandra / Mallick, Amrita / Nawab, Athar / Martin, Rebecca / Shah, Preeya T / Chaudhry, Muhammad / Sigdel, Saroj / El-Hamdani, Mehiar / Liu, Jiang / Xie, Zijian / Abraham, Nader G / Shapiro, Joseph I

Scientific reports

2022 Volume 12, Issue 1, Page(s) 9006

Language	English
Publishing date	2022-05-30
Publishing country	England
Document type	Journal Article ; Retraction of Publication
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-13458-w
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Article ; Online: Retraction Note: The Na/K-ATPase oxidant amplification loop regulates aging.

Sodhi, Komal / Nichols, Alexandra / Mallick, Amrita / Klug, Rebecca L / Liu, Jiang / Wang, Xiaoliang / Srikanthan, Krithika / Goguet-Rubio, Perrine / Nawab, Athar / Pratt, Rebecca / Lilly, Megan N / Sanabria, Juan R / Xie, Zijian / G Abraham, Nader / Shapiro, Joseph I

Scientific reports

2022 Volume 12, Issue 1, Page(s) 9124

Language	English
Publishing date	2022-06-01
Publishing country	England
Document type	Journal Article ; Retraction of Publication
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-13456-y
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Article: Spin Trapping: A Review for the Study of Obesity Related Oxidative Stress and Na

Nawab, Athar / Nichols, Alexandra / Klug, Rebecca / Shapiro, Joseph I / Sodhi, Komal

Journal of clinical & cellular immunology

2017 Volume 8, Issue 3

Abstract: Reactive oxygen species (ROS) have gained attention with mounting evidence of their importance in cell signaling and various disease states. ROS is produced continuously as a natural by-product of normal oxygen metabolism. However, high levels ROS causes ...

Abstract	Reactive oxygen species (ROS) have gained attention with mounting evidence of their importance in cell signaling and various disease states. ROS is produced continuously as a natural by-product of normal oxygen metabolism. However, high levels ROS causes oxidative stress and damage to biomolecules. This results in loss of protein function, DNA cleavage, lipid peroxidation, or ultimately cell injury or death. Obesity has become a worldwide epidemic; studies show fat accumulation is associated with increased ROS and oxidative stress. Evidence exists supporting oxidative stress as a factor driving forward insulin resistance (IR), potentially resulting in diabetes. Na
Language	English
Publishing date	2017-05-17
Publishing country	United States
Document type	Journal Article
ZDB-ID	2684688-3
ISSN	2155-9899
ISSN	2155-9899
DOI	10.4172/2155-9899.1000505
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Article ; Online: Phenotypic Alteration of Hepatocytes in Non-Alcoholic Fatty Liver Disease.

Lakhani, Hari Vishal / Sharma, Dana / Dodrill, Michael W / Nawab, Athar / Sharma, Nitin / Cottrill, Cameron Lee / Shapiro, Joseph I / Sodhi, Komal

International journal of medical sciences

2018 Volume 15, Issue 14, Page(s) 1591–1599

Abstract: Non-Alcoholic Fatty Liver Disease (NAFLD) has been recognized as the most common liver disorder in developed countries. NAFLD progresses from fat accumulation in hepatocytes to steatohepatitis to further stages of fibrosis and cirrhosis. Simple steatosis, ...

Abstract	Non-Alcoholic Fatty Liver Disease (NAFLD) has been recognized as the most common liver disorder in developed countries. NAFLD progresses from fat accumulation in hepatocytes to steatohepatitis to further stages of fibrosis and cirrhosis. Simple steatosis, i.e. fat deposition in the liver, is considered benign and gives way to non-alcoholic steatohepatitis (NASH) with a higher probability of progressing to cirrhosis, and liver-related mortality. Evidence has been found that this progression has been associated with marked alterations in hepatocyte histology and a shift in marker expression of healthy hepatocytes including increased expression of peroxisome proliferator-activated receptor gamma (PPARγ), adipocyte protein (aP2), CD36, interleukin-6 (IL-6), interleukin-18 (IL-18) and adiponectin. This progression shares much in common with the obesity phenotype, which involves a transformation of adipocytes from small, healthy cells to large, dysfunctional ones that contribute to redox imbalance and the progression of metabolic syndrome. Further, activation of Src/ERK signaling via the sodium potassium adenosine triphosphatase (Na/K-ATPase) α-1 subunit in impaired hepatocytes may contribute to redox imbalance, exacerbating the progression of NAFLD. This review hypothesizes that an adipogenic transformation of hepatocytes propagates redox imbalance and that the processes occurring in adipogenesis become activated in fat-laden hepatocytes in liver, thereby driving progression to NAFLD. Further, this review discusses therapeutic interventions to reverse NAFLD including the thiazolidinediones (TZDs) and a variety of antioxidant species. The peptide, pNaKtide, which is an antagonist of Na/K-ATPase signaling, is also proposed as a potential pharmacologic option for reducing reactive oxygen species (ROS) and reversing NAFLD by inhibiting the Na/K-ATPase-modulated ROS amplification loop.
MeSH term(s)	Adipogenesis/drug effects ; Animals ; Antioxidants/pharmacology ; Antioxidants/therapeutic use ; Biomarkers/metabolism ; Disease Models, Animal ; Disease Progression ; Hepatocytes/drug effects ; Hepatocytes/metabolism ; Hepatocytes/pathology ; Humans ; Liver/cytology ; Liver/drug effects ; Liver/metabolism ; Liver/pathology ; Liver Cirrhosis/prevention & control ; MAP Kinase Signaling System ; Non-alcoholic Fatty Liver Disease/drug therapy ; Non-alcoholic Fatty Liver Disease/pathology ; Oxidative Stress/drug effects ; Reactive Oxygen Species/metabolism ; Sodium-Potassium-Exchanging ATPase/metabolism ; Thiazolidinediones/pharmacology ; Thiazolidinediones/therapeutic use
Chemical Substances	Antioxidants ; Biomarkers ; Reactive Oxygen Species ; Thiazolidinediones ; Sodium-Potassium-Exchanging ATPase (EC 3.6.3.9)
Language	English
Publishing date	2018-10-20
Publishing country	Australia
Document type	Journal Article ; Review
ZDB-ID	2151424-0
ISSN	1449-1907 ; 1449-1907
ISSN (online)	1449-1907
ISSN	1449-1907
DOI	10.7150/ijms.27953
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Author Correction: The Adipocyte Na/K-ATPase Oxidant Amplification Loop is the Central Regulator of Western Diet-Induced Obesity and Associated Comorbidities.

Scientific reports

2020 Volume 10, Issue 1, Page(s) 19561

Abstract: An amendment to this paper has been published and can be accessed via a link at the top of the paper. ...

Abstract	An amendment to this paper has been published and can be accessed via a link at the top of the paper.
Language	English
Publishing date	2020-11-05
Publishing country	England
Document type	Published Erratum
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-020-75948-z
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Article ; Online: Central Role for Adipocyte Na,K-ATPase Oxidant Amplification Loop in the Pathogenesis of Experimental Uremic Cardiomyopathy.

Sodhi, Komal / Wang, Xiaoliang / Chaudhry, Muhammad Aslam / Lakhani, Hari Vishal / Zehra, Mishghan / Pratt, Rebecca / Nawab, Athar / Cottrill, Cameron L / Snoad, Brian / Bai, Fang / Denvir, James / Liu, Jiang / Sanabria, Juan R / Xie, Zijian / Abraham, Nader G / Shapiro, Joseph I

publication RETRACTED

Journal of the American Society of Nephrology : JASN

2020 Volume 31, Issue 8, Page(s) 1746–1760

Abstract: Background: Oxidative stress in adipocyte plays a central role in the pathogenesis of obesity as well as in the associated cardiovascular complications. The putative uremic toxin indoxyl sulfate induces oxidative stress and dramatically alters adipocyte ...

Abstract	Background: Oxidative stress in adipocyte plays a central role in the pathogenesis of obesity as well as in the associated cardiovascular complications. The putative uremic toxin indoxyl sulfate induces oxidative stress and dramatically alters adipocyte phenotype Methods: A lentivirus vector introduced the peptide NaKtide with an adiponectin promoter into the mouse model of experimental uremic cardiomyopathy, intraperitoneally. Then adipocyte-specific expression of the peptide was assessed for mice fed a standard diet compared with mice fed a western diet enriched in fat and fructose. Results: Partial nephrectomy induced cardiomyopathy and anemia in the mice, introducing oxidant stress and an altered molecular phenotype of adipocytes that increased production of systemic inflammatory cytokines instead of accumulating lipids, within 4 weeks. Consumption of a western diet significantly worsened the adipocyte oxidant stress, but expression of NaKtide in adipocytes completely prevented the worsening. The peptide-carrying lentivirus achieved comparable expression in skeletal muscle, but did not ameliorate the disease phenotype. Conclusions: Adipocyte-specific expression of NaKtide, introduced with a lentiviral vector, significantly ameliorated adipocyte dysfunction and uremic cardiomyopathy in partially nephrectomized mice. These data suggest that the redox state of adipocytes controls the development of uremic cardiomyopathy in mice subjected to partial nephrectomy. If confirmed in humans, the oxidative state of adipocytes may be a therapeutic target in chronic renal failure.
MeSH term(s)	Adipocytes/metabolism ; Animals ; Apoptosis ; Cardiomyopathies/etiology ; Disease Models, Animal ; Male ; Mice ; Mice, Inbred C57BL ; Nephrectomy ; Oxidative Stress ; Peptide Fragments/physiology ; Sodium-Potassium-Exchanging ATPase/physiology ; Uremia/complications
Chemical Substances	NaKtide ; Peptide Fragments ; Sodium-Potassium-Exchanging ATPase (EC 7.2.2.13)
Language	English
Publishing date	2020-06-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Retracted Publication
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.2019101070
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