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Article ; Online: Targeting Senescent Cells as Therapy for CKD.

Mylonas, Katie J / Ferenbach, David A

Kidney360

2023 Volume 5, Issue 1, Page(s) 142–151

Abstract: Senescent cells accumulate in the kidney with aging, after acute and chronic injuries, and are present in increased numbers in deteriorating kidney transplants. Senescent cells have undergone permanent cell cycle arrest and release many proinflammatory ... ...

Abstract	Senescent cells accumulate in the kidney with aging, after acute and chronic injuries, and are present in increased numbers in deteriorating kidney transplants. Senescent cells have undergone permanent cell cycle arrest and release many proinflammatory cytokines/chemokines and profibrotic factors: the senescence-associated secretory phenotype. Recent work from several groups including our own has shown that senescent cells play a causative role in progression of kidney disease. Experimental evidence also indicates that targeting senescent cells has potential to alter the renal regenerative response, reducing progressive fibrosis and improving functional recovery after injury. Research and clinical interest is focused on understanding how accumulating chronic senescent cells link acute injury to progressive fibrosis, dysfunction, and mortality in human CKD. In this review, we outline current protocols for the identification of how senescent cells are identified in vitro and in vivo . We discuss the proposed mechanisms of actions of first-generation senolytic and senomorphic agents, such as ABT-263 (navitoclax) which targets the BCL2 family of survival factors, and senomorphic agents such as metformin which targets aspects of the senescence-associated secretory phenotype. We also review that emerging technologies, such as nanocarriers, are now being developed to have safer delivery systems for senolytics, greater specificity, fewer off-target effects, and less toxicity. Other methods of senescent cell elimination being developed target various immune evasion tactics displayed by these cells. By understanding the role of senescence in kidney homeostasis and disease, developing new, targeted compounds and the tools to allow their efficacy to be charted noninvasively, it should become possible for senolytic treatments to move from the bench to bedside.
MeSH term(s)	Humans ; Cellular Senescence/physiology ; Senotherapeutics ; Aging/genetics ; Renal Insufficiency, Chronic/therapy ; Fibrosis
Chemical Substances	Senotherapeutics
Language	English
Publishing date	2023-12-05
Publishing country	United States
Document type	Review ; Journal Article
ISSN	2641-7650
ISSN (online)	2641-7650
DOI	10.34067/KID.0000000000000316
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The Role of Ageing and Parenchymal Senescence on Macrophage Function and Fibrosis.

Campbell, Ross A / Docherty, Marie-Helena / Ferenbach, David A / Mylonas, Katie J

Frontiers in immunology

2021 Volume 12, Page(s) 700790

Abstract: In this review, we examine senescent cells and the overlap between the direct biological impact of senescence and the indirect impact senescence ... ...

Abstract	In this review, we examine senescent cells and the overlap between the direct biological impact of senescence and the indirect impact senescence has
MeSH term(s)	Aging/immunology ; Aging/pathology ; Animals ; Cellular Senescence/physiology ; Fibrosis/immunology ; Fibrosis/pathology ; Humans ; Kidney/pathology ; Macrophages
Language	English
Publishing date	2021-06-17
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.700790
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Article: Cellular Senescence and Senotherapies in the Kidney: Current Evidence and Future Directions.

Docherty, Marie Helena / Baird, David P / Hughes, Jeremy / Ferenbach, David A

Frontiers in pharmacology

2020 Volume 11, Page(s) 755

Abstract: Cellular senescence refers to a cellular phenotype characterized by an altered transcriptome, pro-inflammatory secretome, and generally irreversible growth arrest. Acutely senescent cells are widely recognized as performing key physiological ... ...

Abstract	Cellular senescence refers to a cellular phenotype characterized by an altered transcriptome, pro-inflammatory secretome, and generally irreversible growth arrest. Acutely senescent cells are widely recognized as performing key physiological functions
Language	English
Publishing date	2020-05-26
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2020.00755
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Article ; Online: Acute kidney injury and chronic kidney disease: From the laboratory to the clinic.

Ferenbach, David A / Bonventre, Joseph V

Nephrologie & therapeutique

2016 Volume 12 Suppl 1, Page(s) S41–8

Abstract: Chronic kidney disease and acute kidney injury have traditionally been considered as separate entities with different etiologies. This view has changed in recent years, with chronic kidney disease recognized as a major risk factor for the development of ... ...

Abstract	Chronic kidney disease and acute kidney injury have traditionally been considered as separate entities with different etiologies. This view has changed in recent years, with chronic kidney disease recognized as a major risk factor for the development of new acute kidney injury, and acute kidney injury now accepted to lead to de novo or accelerated chronic and end stage kidney diseases. Patients with existing chronic kidney disease appear to be less able to mount a complete 'adaptive' repair after acute insults, and instead repair maladaptively, with accelerated fibrosis and rates of renal functional decline. This article reviews the epidemiological studies in man that have demonstrated the links between these two processes. We also examine clinical and experimental research in areas of importance to both acute and chronic disease: acute and chronic renal injury to the vasculature, the pericyte and leukocyte populations, the signaling pathways implicated in injury and repair, and the impact of cellular stress and increased levels of growth arrested and senescent cells. The importance and therapeutic potential raised by these processes for acute and chronic injury are discussed.
MeSH term(s)	Acute Kidney Injury/complications ; Acute Kidney Injury/epidemiology ; Acute Kidney Injury/pathology ; Disease Progression ; Humans ; Kidney Failure, Chronic/etiology ; Kidney Failure, Chronic/pathology ; Renal Insufficiency, Chronic/epidemiology ; Renal Insufficiency, Chronic/etiology ; Renal Insufficiency, Chronic/pathology ; Risk Factors ; United Kingdom/epidemiology ; United States/epidemiology
Language	English
Publishing date	2016-03-10
Publishing country	France
Document type	Journal Article ; Review
ZDB-ID	2229575-6
ISSN	1872-9177 ; 1769-7255
ISSN (online)	1872-9177
ISSN	1769-7255
DOI	10.1016/j.nephro.2016.02.005
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Zs.A 6298: Show issues

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Article ; Online: Kidney tubules: intertubular, vascular, and glomerular cross-talk.

Ferenbach, David A / Bonventre, Joseph V

Current opinion in nephrology and hypertension

2016 Volume 25, Issue 3, Page(s) 194–202

Abstract: Purpose of review: The kidney mediates the excretion or conservation of water and electrolytes in the face of changing fluid and salt intake and losses. To ultrafilter and reabsorb the exact quantities of free water and salts to maintain euvolemia a ... ...

Abstract	Purpose of review: The kidney mediates the excretion or conservation of water and electrolytes in the face of changing fluid and salt intake and losses. To ultrafilter and reabsorb the exact quantities of free water and salts to maintain euvolemia a range of endocrine, paracrine, and hormonal signaling systems have evolved linking the tubules, capillaries, glomeruli, arterioles, and other intrinsic cells of the kidney. Our understanding of these systems remains incomplete. Recent findings: Recent work has provided new insights into the workings of the communication pathways between tubular segments and the glomeruli and vasculature, with novel therapeutic agents in development. Particular progress has also been made in the visualization of tubuloglomerular feedback. Summary: The review summarizes our current understanding of pathway functions in health and disease, as well as future therapeutic options to protect the healthy and injured kidney.
MeSH term(s)	Capillaries/metabolism ; Homeostasis/physiology ; Humans ; Hypertension/physiopathology ; Kidney Diseases/blood ; Kidney Glomerulus/blood supply ; Kidney Tubules/blood supply
Language	English
Publishing date	2016-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1151092-4
ISSN	1473-6543 ; 1535-3842 ; 1062-4813 ; 1062-4821
ISSN (online)	1473-6543 ; 1535-3842
ISSN	1062-4813 ; 1062-4821
DOI	10.1097/MNH.0000000000000218
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Zs.A 3686: Show issues

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Article ; Online: Mechanisms of maladaptive repair after AKI leading to accelerated kidney ageing and CKD.

Ferenbach, David A / Bonventre, Joseph V

Nature reviews. Nephrology

2015 Volume 11, Issue 5, Page(s) 264–276

Abstract: Acute kidney injury is an increasingly common complication of hospital admission and is associated with high levels of morbidity and mortality. A hypotensive, septic, or toxic insult can initiate a cascade of events, resulting in impaired ... ...

Abstract	Acute kidney injury is an increasingly common complication of hospital admission and is associated with high levels of morbidity and mortality. A hypotensive, septic, or toxic insult can initiate a cascade of events, resulting in impaired microcirculation, activation of inflammatory pathways and tubular cell injury or death. These processes ultimately result in acutely impaired kidney function and initiation of a repair response. This Review explores the various mechanisms responsible for the initiation and propagation of acute kidney injury, the prototypic mechanisms by which a substantially damaged kidney can regenerate its normal architecture, and how the adaptive processes of repair can become maladaptive. These mechanisms, which include G2/M cell-cycle arrest, cell senescence, profibrogenic cytokine production, and activation of pericytes and interstitial myofibroblasts, contribute to the development of progressive fibrotic kidney disease. The end result is a state that mimics accelerated kidney ageing. These mechanisms present important opportunities for the design of targeted therapeutic strategies to promote adaptive renal recovery and minimize progressive fibrosis and chronic kidney disease after acute insults.
MeSH term(s)	Acute Kidney Injury/physiopathology ; Animals ; Cell Cycle Checkpoints/physiology ; Cellular Senescence/physiology ; Fibrosis ; Humans ; Immunity, Cellular ; Kidney/pathology ; Kidney/physiopathology ; Kidney Tubules/physiopathology ; Renal Insufficiency, Chronic/physiopathology
Language	English
Publishing date	2015-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2490366-8
ISSN	1759-507X ; 1759-5061
ISSN (online)	1759-507X
ISSN	1759-5061
DOI	10.1038/nrneph.2015.3
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Zs.A 6334: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Therapeutic Approaches to Aging.

O'Sullivan, Eoin D / Mylonas, Katie J / Ferenbach, David A

JAMA

2019 Volume 321, Issue 9, Page(s) 901

MeSH term(s)	Aging ; Cellular Senescence ; Chronic Disease ; Humans
Language	English
Publishing date	2019-03-05
Publishing country	United States
Document type	Letter ; Comment
ZDB-ID	2958-0
ISSN	1538-3598 ; 0254-9077 ; 0002-9955 ; 0098-7484
ISSN (online)	1538-3598
ISSN	0254-9077 ; 0002-9955 ; 0098-7484
DOI	10.1001/jama.2018.20550
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Article ; Online: Aging modulates the effects of ischemic injury upon mesenchymal cells within the renal interstitium and microvasculature.

Shaw, Isaac W / O'Sullivan, Eoin D / Pisco, Angela O / Borthwick, Gary / Gallagher, Kevin M / Péault, Bruno / Hughes, Jeremy / Ferenbach, David A

Stem cells translational medicine

2021 Volume 10, Issue 8, Page(s) 1232–1248

Abstract: The renal mesenchyme contains heterogeneous cells, including interstitial fibroblasts and pericytes, with key roles in wound healing. Although healing is impaired in aged kidneys, the effect of age and injury on the mesenchyme remains poorly understood. ... ...

Abstract	The renal mesenchyme contains heterogeneous cells, including interstitial fibroblasts and pericytes, with key roles in wound healing. Although healing is impaired in aged kidneys, the effect of age and injury on the mesenchyme remains poorly understood. We characterized renal mesenchymal cell heterogeneity in young vs old animals and after ischemia-reperfusion-injury (IRI) using multiplex immunolabeling and single cell transcriptomics. Expression patterns of perivascular cell markers (α-SMA, CD146, NG2, PDGFR-α, and PDGFR-β) correlated with their interstitial location. PDGFR-α and PDGFR-β co-expression labeled renal myofibroblasts more efficiently than the current standard marker α-SMA, and CD146 was a superior murine renal pericyte marker. Three renal mesenchymal subtypes; pericytes, fibroblasts, and myofibroblasts, were recapitulated with data from two independently performed single cell transcriptomic analyzes of murine kidneys, the first dataset an aging cohort and the second dataset injured kidneys following IRI. Mesenchymal cells segregated into subtypes with distinct patterns of expression with aging and following injury. Baseline uninjured old kidneys resembled post-ischemic young kidneys, with this phenotype further exaggerated following IRI. These studies demonstrate that age modulates renal perivascular/interstitial cell marker expression and transcriptome at baseline and in response to injury and provide tools for the histological and transcriptomic analysis of renal mesenchymal cells, paving the way for more accurate classification of renal mesenchymal cell heterogeneity and identification of age-specific pathways and targets.
MeSH term(s)	Aged ; Aging ; Animals ; Fibrosis ; Humans ; Ischemia/metabolism ; Kidney/pathology ; Mice ; Microvessels ; Myofibroblasts/metabolism ; Pericytes/metabolism ; Reperfusion Injury/metabolism
Language	English
Publishing date	2021-05-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2642270-0
ISSN	2157-6580 ; 2157-6580
ISSN (online)	2157-6580
ISSN	2157-6580
DOI	10.1002/sctm.20-0392
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Article ; Online: Renal Aging: Causes and Consequences.

O'Sullivan, Eoin D / Hughes, Jeremy / Ferenbach, David A

Journal of the American Society of Nephrology : JASN

2016 Volume 28, Issue 2, Page(s) 407–420

Abstract: Individuals age >65 years old are the fastest expanding population demographic throughout the developed world. Consequently, more aged patients than before are receiving diagnoses of impaired renal function and nephrosclerosis-age-associated histologic ... ...

Abstract	Individuals age >65 years old are the fastest expanding population demographic throughout the developed world. Consequently, more aged patients than before are receiving diagnoses of impaired renal function and nephrosclerosis-age-associated histologic changes in the kidneys. Recent studies have shown that the aged kidney undergoes a range of structural changes and has altered transcriptomic, hemodynamic, and physiologic behavior at rest and in response to renal insults. These changes impair the ability of the kidney to withstand and recover from injury, contributing to the high susceptibility of the aged population to AKI and their increased propensity to develop subsequent progressive CKD. In this review, we examine these features of the aged kidney and explore the various validated and putative pathways contributing to the changes observed with aging in both experimental animal models and humans. We also discuss the potential for additional study to increase understanding of the aged kidney and lead to novel therapeutic strategies.
MeSH term(s)	Aging ; Biomedical Research/trends ; Cell Cycle ; Cell Hypoxia ; Forecasting ; Humans ; Kidney/cytology ; Kidney/pathology ; Kidney/physiology ; Kidney/physiopathology ; Male ; Oxidative Stress ; Renal Insufficiency, Chronic/etiology ; Signal Transduction
Language	English
Publishing date	2016-11-15
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.2015121308
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Zs.A 3344: Show issues

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Article ; Online: Cellular Senescence in the Kidney.

Docherty, Marie-Helena / O'Sullivan, Eoin D / Bonventre, Joseph V / Ferenbach, David A

Journal of the American Society of Nephrology : JASN

2019 Volume 30, Issue 5, Page(s) 726–736

Abstract: Senescent cells have undergone permanent growth arrest, adopt an altered secretory phenotype, and accumulate in the kidney and other organs with ageing and injury. Senescence has diverse physiologic roles and experimental studies support its importance ... ...

Abstract	Senescent cells have undergone permanent growth arrest, adopt an altered secretory phenotype, and accumulate in the kidney and other organs with ageing and injury. Senescence has diverse physiologic roles and experimental studies support its importance in nephrogenesis, successful tissue repair, and in opposing malignant transformation. However, recent murine studies have shown that depletion of chronically senescent cells extends healthy lifespan and delays age-associated disease-implicating senescence and the senescence-associated secretory phenotype as drivers of organ dysfunction. Great interest is therefore focused on the manipulation of senescence as a novel therapeutic target in kidney disease. In this review, we examine current knowledge and areas of ongoing uncertainty regarding senescence in the human kidney and experimental models. We summarize evidence supporting the role of senescence in normal kidney development and homeostasis but also senescence-induced maladaptive repair, renal fibrosis, and transplant failure. Recent studies using senescent cell manipulation and depletion as novel therapies to treat renal disease are discussed, and we explore unanswered questions for future research.
MeSH term(s)	Aging/genetics ; Aging/physiology ; Animals ; Cellular Senescence/genetics ; Cellular Senescence/physiology ; Humans ; Kidney/pathology ; Kidney/physiopathology ; Mice ; Models, Animal ; Prognosis ; Renal Insufficiency, Chronic/mortality ; Renal Insufficiency, Chronic/pathology ; Renal Insufficiency, Chronic/therapy
Language	English
Publishing date	2019-04-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.2018121251
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