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Article ; Online: Autophagy and mitophagy: physiological implications in kidney inflammation and diseases.

Bhatia, Divya / Choi, Mary E

American journal of physiology. Renal physiology

2023 Volume 325, Issue 1, Page(s) F1–F21

Abstract: Autophagy is a ubiquitous intracellular cytoprotective quality control program that maintains cellular homeostasis by recycling superfluous cytoplasmic components (lipid droplets, protein, or glycogen aggregates) and invading pathogens. Mitophagy is a ... ...

Abstract	Autophagy is a ubiquitous intracellular cytoprotective quality control program that maintains cellular homeostasis by recycling superfluous cytoplasmic components (lipid droplets, protein, or glycogen aggregates) and invading pathogens. Mitophagy is a selective form of autophagy that by recycling damaged mitochondrial material, which can extracellularly act as damage-associated molecular patterns, prevents their release. Autophagy and mitophagy are indispensable for the maintenance of kidney homeostasis and exert crucial functions during both physiological and disease conditions. Impaired autophagy and mitophagy can negatively impact the pathophysiological state and promote its progression. Autophagy helps in maintaining structural integrity of the kidney. Mitophagy-mediated mitochondrial quality control is explicitly critical for regulating cellular homeostasis in the kidney. Both autophagy and mitophagy attenuate inflammatory responses in the kidney. An accumulating body of evidence highlights that persistent kidney injury-induced oxidative stress can contribute to dysregulated autophagic and mitophagic responses and cell death. Autophagy and mitophagy also communicate with programmed cell death pathways (apoptosis and necroptosis) and play important roles in cell survival by preventing nutrient deprivation and regulating oxidative stress. Autophagy and mitophagy are activated in the kidney after acute injury. However, their aberrant hyperactivation can be deleterious and cause tissue damage. The findings on the functions of autophagy and mitophagy in various models of chronic kidney disease are heterogeneous and cell type- and context-specific dependent. In this review, we discuss the roles of autophagy and mitophagy in the kidney in regulating inflammatory responses and during various pathological manifestations.
MeSH term(s)	Humans ; Mitophagy ; Autophagy/physiology ; Nephritis ; Kidney ; Inflammation
Language	English
Publishing date	2023-05-11
Publishing country	United States
Document type	Journal Article ; Review ; 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.00012.2023
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Article ; Online: Autophagy in Kidney Disease.

Choi, Mary E

Annual review of physiology

2019 Volume 82, Page(s) 297–322

Abstract: Autophagy is a cellular homeostatic program for the turnover of cellular organelles and proteins, in which double-membraned vesicles (autophagosomes) sequester cytoplasmic cargos, which are subsequently delivered to the lysosome for degradation. Emerging ...

Abstract	Autophagy is a cellular homeostatic program for the turnover of cellular organelles and proteins, in which double-membraned vesicles (autophagosomes) sequester cytoplasmic cargos, which are subsequently delivered to the lysosome for degradation. Emerging evidence implicates autophagy as an important modulator of human disease. Macroautophagy and selective autophagy (e.g., mitophagy, aggrephagy) can influence cellular processes, including cell death, inflammation, and immune responses, and thereby exert both adaptive and maladaptive roles in disease pathogenesis. Autophagy has been implicated in acute kidney injury, which can arise in response to nephrotoxins, sepsis, and ischemia/reperfusion, and in chronic kidney diseases. The latter includes comorbidities of diabetes and recent evidence for chronic obstructive pulmonary disease-associated kidney injury. Roles of autophagy in polycystic kidney disease and kidney cancer have also been described. Targeting the autophagy pathway may have therapeutic benefit in the treatment of kidney disorders.
MeSH term(s)	Animals ; Autophagy ; Humans ; Kidney Diseases/pathology ; Mitophagy ; Renal Insufficiency, Chronic/pathology
Language	English
Publishing date	2019-10-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	207933-1
ISSN	1545-1585 ; 0066-4278
ISSN (online)	1545-1585
ISSN	0066-4278
DOI	10.1146/annurev-physiol-021119-034658
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Article ; Online: Novel Roles of Necroptosis Mediator Receptor-Interacting Protein Kinase 3 in Kidney Injury.

Uni, Rie / Choi, Mary E

Nephron

2021 Volume 146, Issue 3, Page(s) 259–263

Abstract: Necroptosis is a programmed cell death that is characterized by regulated necrosis resulting in plasma membrane rupture and subsequent release of damage-associated molecular patterns (DAMPs). Receptor-interacting protein kinase 3 (RIPK3) is a key ... ...

Abstract	Necroptosis is a programmed cell death that is characterized by regulated necrosis resulting in plasma membrane rupture and subsequent release of damage-associated molecular patterns (DAMPs). Receptor-interacting protein kinase 3 (RIPK3) is a key mediator of this pathway. Accumulating evidence supports a critical role of RIPK3 and the necroptosis pathway in various human diseases. In this review, we discuss recent investigations that have uncovered pathogenic roles of RIPK3 in both acute kidney injury (AKI) and kidney fibrosis. RIPK3 promotes kidney tubular injury via a mechanism involving mitochondrial dysfunction. Additionally, extracellular mitochondrial DNA, which is one of the necroptotic DAMPs, released from damaged mitochondria correlates with kidney tubular injury and represents a potential novel biomarker. RIPK3 also induces kidney fibrogenesis through AKT-dependent activation of the metabolic enzyme ATP citrate lyase. Thus, the RIPK3-mediated necroptosis pathway may serve as a promising new therapeutic target in AKI and kidney fibrosis.
MeSH term(s)	Acute Kidney Injury/pathology ; Apoptosis ; Female ; Fibrosis ; Humans ; Kidney/pathology ; Male ; Necroptosis ; Necrosis/pathology
Language	English
Publishing date	2021-07-20
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	207121-6
ISSN	2235-3186 ; 1423-0186 ; 1660-8151 ; 0028-2766
ISSN (online)	2235-3186 ; 1423-0186
ISSN	1660-8151 ; 0028-2766
DOI	10.1159/000517732
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Article ; Online: The Emerging Role of Mitophagy in Kidney Diseases.

Bhatia, Divya / Choi, Mary E

Journal of life sciences (Westlake Village, Calif.)

2020 Volume 1, Issue 3, Page(s) 13–22

Abstract: Mitochondria fulfill the high metabolic energy demands of the kidney and are regularly exposed to oxidative stress causing mitochondrial damage. The selective removal of damaged and dysfunctional mitochondria through a process known as mitophagy is ... ...

Abstract	Mitochondria fulfill the high metabolic energy demands of the kidney and are regularly exposed to oxidative stress causing mitochondrial damage. The selective removal of damaged and dysfunctional mitochondria through a process known as mitophagy is essential in maintaining cellular homeostasis and physiological function. Mitochondrial quality control by mitophagy is particularly crucial for an organ such as the kidney, which is rich in mitochondria. The role of mitophagy in the pathogenesis of kidney diseases has lately gained significant attention. In this review, we summarize the current understanding of the implications of mitophagy during pathological conditions of the kidney, including acute and chronic kidney diseases.
Language	English
Publishing date	2020-02-19
Publishing country	United States
Document type	Journal Article
ISSN	2688-1020
ISSN (online)	2688-1020
DOI	10.36069/jols/20191203
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Article ; Online: Autophagy in kidney disease: Advances and therapeutic potential.

Bhatia, Divya / Choi, Mary E

Progress in molecular biology and translational science

2020 Volume 172, Page(s) 107–133

Abstract: Autophagy is a highly conserved intracellular catabolic process for the degradation of cytoplasmic components that has recently gained increasing attention for its importance in kidney diseases. It is indispensable for the maintenance of kidney ... ...

Abstract	Autophagy is a highly conserved intracellular catabolic process for the degradation of cytoplasmic components that has recently gained increasing attention for its importance in kidney diseases. It is indispensable for the maintenance of kidney homeostasis both in physiological and pathological conditions. Investigations utilizing various kidney cell-specific conditional autophagy-related gene knockouts have facilitated the advancement in understanding of the role of autophagy in the kidney. Recent findings are raising the possibility that defective autophagy exerts a critical role in different pathological conditions of the kidney. An emerging body of evidence reveals that autophagy exhibits cytoprotective functions in both glomerular and tubular compartments of the kidney, suggesting the upregulation of autophagy as an attractive therapeutic strategy. However, there is also accumulating evidence that autophagy could be deleterious, which presents a formidable challenge in developing therapeutic strategies targeting autophagy. Here, we review the recent advances in research on the role of autophagy during different pathological conditions, including acute kidney injury (AKI), focusing on sepsis, ischemia-reperfusion injury, cisplatin, and heavy metal-induced AKI. We also discuss the role of autophagy in chronic kidney disease (CKD) focusing on the pathogenesis of tubulointerstitial fibrosis, podocytopathies including focal segmental glomerulosclerosis, diabetic nephropathy, IgA nephropathy, membranous nephropathy, HIV-associated nephropathy, and polycystic kidney disease.
MeSH term(s)	Animals ; Autophagy/physiology ; Autophagy-Related Proteins/physiology ; Cisplatin/toxicity ; Clinical Trials as Topic ; Disease Models, Animal ; Homeostasis ; Humans ; Kidney Diseases/chemically induced ; Kidney Diseases/drug therapy ; Kidney Diseases/physiopathology ; Kidney Glomerulus/physiology ; Kidney Tubules/physiology ; Lysosomes/physiology ; Metals, Heavy/toxicity ; Mice ; Mice, Knockout ; Nephrosis, Lipoid/pathology ; Podocytes/pathology ; TOR Serine-Threonine Kinases/antagonists & inhibitors ; TOR Serine-Threonine Kinases/physiology
Chemical Substances	Autophagy-Related Proteins ; Metals, Heavy ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2020-02-03
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2471995-X
ISSN	1878-0814 ; 0079-6603 ; 1877-1173
ISSN (online)	1878-0814
ISSN	0079-6603 ; 1877-1173
DOI	10.1016/bs.pmbts.2020.01.008
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Article ; Online: Retinoic acid receptor α activity in proximal tubules prevents kidney injury and fibrosis.

DiKun, Krysta M / Tang, Xiao-Han / Fu, Leiping / Choi, Mary E / Lu, Changyuan / Gudas, Lorraine J

Proceedings of the National Academy of Sciences of the United States of America

2024 Volume 121, Issue 7, Page(s) e2311803121

Abstract: Chronic kidney disease (CKD) is characterized by a gradual loss of kidney function and affects ~13.4% of the global population. Progressive tubulointerstitial fibrosis, driven in part by proximal tubule (PT) damage, is a hallmark of late stages of CKD ... ...

Abstract	Chronic kidney disease (CKD) is characterized by a gradual loss of kidney function and affects ~13.4% of the global population. Progressive tubulointerstitial fibrosis, driven in part by proximal tubule (PT) damage, is a hallmark of late stages of CKD and contributes to the development of kidney failure, for which there are limited treatment options. Normal kidney development requires signaling by vitamin A (retinol), which is metabolized to retinoic acid (RA), an endogenous agonist for the RA receptors (RARα, β, γ). RARα levels are decreased in a mouse model of diabetic nephropathy and restored with RA administration; additionally, RA treatment reduced fibrosis. We developed a mouse model in which a spatiotemporal (tamoxifen-inducible) deletion of RARα in kidney PT cells of adult mice causes mitochondrial dysfunction, massive PT injury, and apoptosis without the use of additional nephrotoxic substances. Long-term effects (3 to 4.5 mo) of RARα deletion include increased PT secretion of transforming growth factor β1, inflammation, interstitial fibrosis, and decreased kidney function, all of which are major features of human CKD. Therefore, RARα's actions in PTs are crucial for PT homeostasis, and loss of RARα causes injury and a key CKD phenotype.
MeSH term(s)	Animals ; Humans ; Mice ; Disease Models, Animal ; Fibrosis ; Kidney/metabolism ; Kidney Tubules, Proximal/metabolism ; Renal Insufficiency, Chronic/genetics ; Renal Insufficiency, Chronic/prevention & control ; Retinoic Acid Receptor alpha/genetics ; Retinoic Acid Receptor alpha/metabolism ; Tretinoin/pharmacology ; Tretinoin/metabolism
Chemical Substances	Retinoic Acid Receptor alpha ; Tretinoin (5688UTC01R) ; Rara protein, mouse
Language	English
Publishing date	2024-02-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2311803121
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Article ; Online: Autophagy in chronic lung disease.

Racanelli, Alexandra C / Choi, Augustine M K / Choi, Mary E

Progress in molecular biology and translational science

2020 Volume 172, Page(s) 135–156

Abstract: The development of chronic lung disease occurs as a consequence of multiple cellular events that involve an initial insult which often leads to the development of chronic inflammation, and the dysregulation of cellular proliferation and cell death ... ...

Abstract	The development of chronic lung disease occurs as a consequence of multiple cellular events that involve an initial insult which often leads to the development of chronic inflammation, and the dysregulation of cellular proliferation and cell death mechanisms. Multiple cell types in the lung are key to the respiratory and protective/barrier functions necessary to manage the chronic exposures to environmental, mechanical, and oxidative stressors. Autophagy is essential to lung development and homeostasis, as well as the prevention and development of disease. The cellular process involves the collection and removal of unwanted organelles and proteins through lysosomal degradation. In recent years, investigations have addressed the roles of autophagy and selective autophagy in numerous chronic lung diseases. Here, we highlight recent advances on the role of autophagy in the pathogenesis of asthma, chronic obstructive pulmonary disease and emphysema, pulmonary arterial hypertension, and idiopathic pulmonary fibrosis.
MeSH term(s)	Animals ; Autophagosomes/physiology ; Autophagy ; Cigarette Smoking/pathology ; Disease Models, Animal ; Homeostasis ; Humans ; Inflammation/pathology ; Lung/growth & development ; Lung Diseases/etiology ; Lung Diseases/pathology ; Lysosomes/physiology ; Mice ; Mice, Knockout ; Organelles ; Stress, Physiological ; TOR Serine-Threonine Kinases/antagonists & inhibitors
Chemical Substances	MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1)
Language	English
Publishing date	2020-03-12
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2471995-X
ISSN	1878-0814 ; 0079-6603 ; 1877-1173
ISSN (online)	1878-0814
ISSN	0079-6603 ; 1877-1173
DOI	10.1016/bs.pmbts.2020.02.001
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Article: Mitochondrial dysfunction in kidney injury, inflammation, and disease: Potential therapeutic approaches.

Bhatia, Divya / Capili, Allyson / Choi, Mary E

Kidney research and clinical practice

2020 Volume 39, Issue 3, Page(s) 244–258

Abstract: Mitochondria are energy-producing organelles that not only satisfy the high metabolic demands of the kidney but sense and respond to kidney injury-induced oxidative stress and inflammation. Kidneys are rich in mitochondria. Mitochondrial dysfunction ... ...

Abstract	Mitochondria are energy-producing organelles that not only satisfy the high metabolic demands of the kidney but sense and respond to kidney injury-induced oxidative stress and inflammation. Kidneys are rich in mitochondria. Mitochondrial dysfunction plays a critical role in the progression of acute kidney injury and chronic kidney disease. Mitochondrial responses to specific stimuli are highly regulated and synergistically modulated by tightly interconnected processes, including mitochondrial dynamics (fission, fusion) and mitophagy. The counterbalance between these processes is essential in maintaining a healthy network of mitochondria. Recent literature suggests that alterations in mitochondrial dynamics are implicated in kidney injury and the progression of kidney diseases. A decrease in mitochondrial fusion promotes fission-induced mitochondrial fragmentation, but a reduction in mitochondrial fission produces excessive mitochondrial elongation. The removal of dysfunctional mitochondria by mitophagy is crucial for their quality control. Defective mitochondrial function disrupts cellular redox potential and can cause cell death. Mitochondrial DNA derived from damaged cells also act as damage-associated molecular patterns to recruit immune cells and the inflammatory response can further exaggerate kidney injury. This review provides a comprehensive overview of the role of mitochondrial dysfunction in acute kidney injury and chronic kidney disease. We discuss the processes that control mitochondrial stress responses to kidney injury and review recent advances in understanding the role of mitochondrial dysfunction in inflammation and tissue damage through the use of different experimental models of kidney disease. We also describe potential mitochondria-targeted therapeutic approaches.
Language	English
Publishing date	2020-08-28
Publishing country	Korea (South)
Document type	Journal Article ; Review
ZDB-ID	2656420-8
ISSN	2211-9132
ISSN	2211-9132
DOI	10.23876/j.krcp.20.082
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Article ; Online: REIN on obesity, proteinuria and CKD.

Choi, Mary E

Journal of the American Society of Nephrology : JASN

2011 Volume 22, Issue 6, Page(s) 990–992

MeSH term(s)	Angiotensin-Converting Enzyme Inhibitors/pharmacology ; Angiotensin-Converting Enzyme Inhibitors/therapeutic use ; Body Mass Index ; Chronic Disease ; Comorbidity ; Creatinine/blood ; Disease Progression ; Glomerular Filtration Rate/drug effects ; Glomerular Filtration Rate/physiology ; Humans ; Kidney Diseases/drug therapy ; Kidney Diseases/epidemiology ; Kidney Diseases/physiopathology ; Kidney Failure, Chronic/prevention & control ; Obesity/complications ; Obesity/physiopathology ; Proteinuria/drug therapy ; Proteinuria/epidemiology ; Proteinuria/physiopathology ; Ramipril/pharmacology ; Ramipril/therapeutic use ; Treatment Outcome
Chemical Substances	Angiotensin-Converting Enzyme Inhibitors ; Creatinine (AYI8EX34EU) ; Ramipril (L35JN3I7SJ)
Language	English
Publishing date	2011-06
Publishing country	United States
Document type	Comment ; Editorial
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.2011040423
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Article ; Online: Autophagy: A Lysosome-Dependent Process with Implications in Cellular Redox Homeostasis and Human Disease.

Ryter, Stefan W / Bhatia, Divya / Choi, Mary E

Antioxidants & redox signaling

2018 Volume 30, Issue 1, Page(s) 138–159

Abstract: Significance: Autophagy, a lysosome-dependent homeostatic process inherent to cells and tissues, has emerging significance in the pathogenesis of human disease. This process enables the degradation and turnover of cytoplasmic substrates via membrane- ... ...

Abstract	Significance: Autophagy, a lysosome-dependent homeostatic process inherent to cells and tissues, has emerging significance in the pathogenesis of human disease. This process enables the degradation and turnover of cytoplasmic substrates via membrane-dependent sequestration in autophagic vesicles (autophagosomes) and subsequent lysosomal delivery of cargo. Recent Advances: Selective forms of autophagy can target specific substrates (e.g., organelles, protein aggregates, and lipids) for processing. Autophagy is highly regulated by oxidative stress, including exposure to altered oxygen tension, by direct and indirect mechanisms, and contributes to inducible defenses against oxidative stress. Mitochondrial autophagy (mitophagy) plays a critical role in the oxidative stress response, through maintenance of mitochondrial integrity. Critical issues: Autophagy can impact a number of vital cellular processes including inflammation and adaptive immunity, host defense, lipid metabolism and storage, mitochondrial homeostasis, and clearance of aggregated proteins, all which may be of significance in human disease. Autophagy can exert both maladaptive and adaptive roles in disease pathogenesis, which may also be influenced by autophagy impairment. This review highlights the essential roles of autophagy in human diseases, with a focus on diseases in which oxidative stress or inflammation play key roles, including human lung, liver, kidney and heart diseases, metabolic diseases, and diseases of the cardiovascular and neural systems. Future directions: Investigations that further elucidate the complex role of autophagy in the pathogenesis of disease will facilitate targeting this pathway for therapies in specific diseases.
MeSH term(s)	Animals ; Autophagy ; Cardiovascular Diseases/metabolism ; Cardiovascular Diseases/pathology ; Heart Diseases/metabolism ; Heart Diseases/pathology ; Homeostasis ; Humans ; Kidney Diseases/metabolism ; Kidney Diseases/pathology ; Liver Diseases/metabolism ; Liver Diseases/pathology ; Lung Diseases/metabolism ; Lung Diseases/pathology ; Lysosomes/metabolism ; Metabolic Diseases/metabolism ; Metabolic Diseases/pathology ; Oxidation-Reduction
Language	English
Publishing date	2018-03-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2018.7518
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