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Article ; Online: Tackling AKI.

Rana, Rajashree / Breyer, Matthew D

Journal of the American Society of Nephrology : JASN

2023 Volume 34, Issue 6, Page(s) 935–936

MeSH term(s)	Humans ; Acute Kidney Injury
Language	English
Publishing date	2023-04-21
Publishing country	United States
Document type	Research Support, Non-U.S. Gov't ; Editorial ; Comment
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.0000000000000140
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Article ; Online: The Use of Genomics to Drive Kidney Disease Drug Discovery and Development.

Reilly, Dermot F / Breyer, Matthew D

Clinical journal of the American Society of Nephrology : CJASN

2020 Volume 15, Issue 9, Page(s) 1342–1351

Abstract: As opposed to diseases such as cancer, autoimmune disease, and diabetes, identifying drugs to treat CKD has proven significantly more challenging. Over the past 2 decades, new potential therapeutic targets have been identified as genetically altered ... ...

Abstract	As opposed to diseases such as cancer, autoimmune disease, and diabetes, identifying drugs to treat CKD has proven significantly more challenging. Over the past 2 decades, new potential therapeutic targets have been identified as genetically altered proteins involved in rare monogenetic kidney diseases. Other possible target genes have been implicated through common genetic polymorphisms associated with CKD in the general population. Significant challenges remain before translating these genetic insights into clinical therapies for CKD. This paper will discuss how genetic variants may be leveraged to develop drugs and will especially focus on those genes associated with CKD to exemplify the value and challenges in including genetic information in the drug development pipeline.
MeSH term(s)	Animals ; Drug Development ; Drug Discovery ; Genetic Predisposition to Disease ; Genomics ; Humans ; Mutation ; Phenotype ; Polymorphism, Genetic ; Renal Agents/adverse effects ; Renal Agents/therapeutic use ; Renal Insufficiency, Chronic/diagnosis ; Renal Insufficiency, Chronic/drug therapy ; Renal Insufficiency, Chronic/genetics
Chemical Substances	Renal Agents
Language	English
Publishing date	2020-03-19
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2226665-3
ISSN	1555-905X ; 1555-9041
ISSN (online)	1555-905X
ISSN	1555-9041
DOI	10.2215/CJN.11070919
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Article: Cyclooxygenase-2 contributes to diabetic nephropathy through glomerular EP4 receptor.

Guan, Yi / Davis, Linda / Breyer, Matthew D / Hao, Chuan-Ming

Prostaglandins & other lipid mediators

2022 Volume 159, Page(s) 106621

Abstract: Diabetic nephropathy (DN) is a major microvascular complication of diabetes and the leading cause of mortality in diabetic patients. Cyclooxygenase (COX) and COX-derived prostanoids are documented to participate in the pathogenesis of diabetic ... ...

Abstract	Diabetic nephropathy (DN) is a major microvascular complication of diabetes and the leading cause of mortality in diabetic patients. Cyclooxygenase (COX) and COX-derived prostanoids are documented to participate in the pathogenesis of diabetic nephropathy. Herein, we found an increased COX2 expression level in diabetic kidneys of STZ-induced DBA mice. The COX2 inhibitor significantly attenuated albuminuria and histological lesions, accompanied by up-regulation of the renal angiopoietin-1/tie-2 system. This finding is consistent with the presence of an angiogenic signature in endothelial cells during the development of DN. Prostaglandin E2 (PGE2) is the most abundant prostanoid in the kidney, and its receptor EP4 is expressed in the glomerulus, as determined by in situ hybridization. To test the hypothesis that diabetes-associated COX2 overexpression induces renal PGE2 production and endothelial dysfunction by activating glomerular EP4 receptors, the effect of an EP4 antagonist on Akita/DBA mice was investigated. Our results showed that blockade of EP4 receptor significantly reduced albuminuria in diabetic mice. Owing to the established adverse effect of COX2 inhibitors, our study provided new insight into meaningful renal benefits for diabetic nephropathy by targeting the EP4 receptor.
MeSH term(s)	Albuminuria ; Animals ; Cyclooxygenase 2 ; Cyclooxygenase 2 Inhibitors ; Diabetes Mellitus, Experimental/complications ; Diabetic Nephropathies ; Dinoprostone ; Endothelial Cells ; Female ; Humans ; Male ; Mice ; Mice, Inbred DBA ; Prostaglandins ; Receptors, Prostaglandin E, EP4 Subtype
Chemical Substances	Cyclooxygenase 2 Inhibitors ; Prostaglandins ; Receptors, Prostaglandin E, EP4 Subtype ; Cyclooxygenase 2 (EC 1.14.99.1) ; Dinoprostone (K7Q1JQR04M)
Language	English
Publishing date	2022-02-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1426962-4
ISSN	2212-196X ; 1098-8823 ; 0090-6980
ISSN (online)	2212-196X
ISSN	1098-8823 ; 0090-6980
DOI	10.1016/j.prostaglandins.2022.106621
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Article ; Online: Improving productivity of modern-day drug discovery.

Breyer, Matthew D

Expert opinion on drug discovery

2014 Volume 9, Issue 2, Page(s) 115–118

Abstract: The pharmaceutical industry is confronted by increasing costs of clinical development and diminishing productivity. The most challenging aspect of drug development has been the failure of therapeutics in expensive Phase II or III trials, and this is most ...

Abstract	The pharmaceutical industry is confronted by increasing costs of clinical development and diminishing productivity. The most challenging aspect of drug development has been the failure of therapeutics in expensive Phase II or III trials, and this is most commonly due to lack of efficacy. More can be done during the drug discovery phase to optimize efficacy-testing in animal models by expending resources to explore the congruence of the animal model with the human disease. Historically, relatively little attention has been paid to validation of these models, but access to molecular mRNA and genetic profiling offers a new lens through which the similarity of these disease models to human diseases can be examined and their utility for exploring therapeutic efficacy can be optimized. Exploring congruent experimental end points in clinical and preclinical experiments will also increase confidence of success in late phase clinical development. The expense of this investment is trivial compared to the costs of a failed clinical trial, more than justifying this endeavor.
MeSH term(s)	Animals ; Disease Models, Animal ; Drug Discovery ; Drug Industry ; Humans
Language	English
Publishing date	2014-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2259618-5
ISSN	1746-045X ; 1746-0441
ISSN (online)	1746-045X
ISSN	1746-0441
DOI	10.1517/17460441.2014.870150
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Article ; Online: Mapping the single-cell transcriptomic response of murine diabetic kidney disease to therapies.

Wu, Haojia / Gonzalez Villalobos, Romer / Yao, Xiang / Reilly, Dermot / Chen, Tao / Rankin, Matthew / Myshkin, Eugene / Breyer, Matthew D / Humphreys, Benjamin D

Cell metabolism

2022 Volume 34, Issue 7, Page(s) 1064–1078.e6

Abstract: Diabetic kidney disease (DKD) occurs in ∼40% of patients with diabetes and causes kidney failure, cardiovascular disease, and premature death. We analyzed the response of a murine DKD model to five treatment regimens using single-cell RNA sequencing ( ... ...

Abstract	Diabetic kidney disease (DKD) occurs in ∼40% of patients with diabetes and causes kidney failure, cardiovascular disease, and premature death. We analyzed the response of a murine DKD model to five treatment regimens using single-cell RNA sequencing (scRNA-seq). Our atlas of ∼1 million cells revealed a heterogeneous response of all kidney cell types both to DKD and its treatment. Both monotherapy and combination therapies targeted differing cell types and induced distinct and non-overlapping transcriptional changes. The early effects of sodium-glucose cotransporter-2 inhibitors (SGLT2i) on the S1 segment of the proximal tubule suggest that this drug class induces fasting mimicry and hypoxia responses. Diabetes downregulated the spliceosome regulator serine/arginine-rich splicing factor 7 (Srsf7) in proximal tubule that was specifically rescued by SGLT2i. In vitro proximal tubule knockdown of Srsf7 induced a pro-inflammatory phenotype, implicating alternative splicing as a driver of DKD and suggesting SGLT2i regulation of proximal tubule alternative splicing as a potential mechanism of action for this drug class.
MeSH term(s)	Animals ; Cardiovascular Diseases/drug therapy ; Diabetes Mellitus, Type 2/metabolism ; Diabetic Nephropathies/drug therapy ; Diabetic Nephropathies/genetics ; Mice ; Sodium-Glucose Transporter 2 Inhibitors/pharmacology ; Sodium-Glucose Transporter 2 Inhibitors/therapeutic use ; Transcriptome/genetics
Chemical Substances	Sodium-Glucose Transporter 2 Inhibitors
Language	English
Publishing date	2022-06-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2022.05.010
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Article ; Online: Prostacyclin Mitigates Renal Fibrosis by Activating Fibroblast Prostaglandin I 2 Receptor.

Li, Jing / Guan, Yi / Xu, Yunyu / Cao, Yingxue / Xie, Qionghong / Harris, Raymond C / Breyer, Matthew D / Lu, Limin / Hao, Chuan-Ming

Journal of the American Society of Nephrology : JASN

2023 Volume 35, Issue 2, Page(s) 149–165

Abstract: Significance statement: Renal fibrosis is a common pathologic process of progressive CKD. We have provided strong evidence that PGI 2 is an important component in the kidney injury/repairing process by reducing fibrosis and protecting renal function ... ...

Abstract	Significance statement: Renal fibrosis is a common pathologic process of progressive CKD. We have provided strong evidence that PGI 2 is an important component in the kidney injury/repairing process by reducing fibrosis and protecting renal function from declining. In our study, administration of a PGI 2 analog or selective PTGIR agonist after the acute injury ameliorated renal fibrosis. Our findings provide new insights into the role of PGI 2 in kidney biology and suggest that targeting PGI 2 /PTGIR may be a potential therapeutic strategy for CKD. Background: Prostanoids have been demonstrated to be important modulators to maintain tissue homeostasis in response to physiologic or pathophysiologic stress. Prostacyclin (PGI 2 ) is a member of prostanoids. While limited studies have shown that PGI 2 is involved in the tissue injury/repairing process, its role in renal fibrosis and CKD progression requires further investigation. Methods: Prostacyclin synthase ( Ptgis )-deficient mice, prostaglandin I 2 receptor ( Ptgir )-deficient mice, and an oral PGI 2 analog and selective PTGIR agonist were used to examine the role of PGI 2 in renal fibrosis in mouse models. We also analyzed the single-cell RNA-Seq data to examine the PTGIR -expressing cells in the kidneys of patients with CKD. Results: Increased PTGIS expression has been observed in fibrotic kidneys in both humans and mice. Deletion of the PTGIS gene aggravated renal fibrosis and decline of renal function in murine models. A PGI 2 analog or PTGIR agonist that was administered after the acute injury ameliorated renal fibrosis. PTGIR, the PGI 2 receptor, deficiency blunted the protective effect of the PGI 2 analog. Fibroblasts and myofibroblasts were the major cell types expressing PTGIR in the kidneys of patients with CKD. Deletion of PTGIR in collagen-producing fibroblastic cells aggravated renal fibrosis. The protective effect of PGI 2 was associated with the inhibition of fibroblast activation through PTGIR-mediated signaling. Conclusions: PGI 2 is an important component in the kidney injury/repairing process by preventing the overactivation of fibroblasts during the repairing process and protecting the kidney from fibrosis and decline of renal function. Our findings suggest that PGI 2 /PTGIR is a potential therapeutic target for CKD.
MeSH term(s)	Humans ; Animals ; Mice ; Epoprostenol/pharmacology ; Epoprostenol/metabolism ; Prostaglandins I ; Kidney/metabolism ; Renal Insufficiency, Chronic/drug therapy ; Renal Insufficiency, Chronic/etiology ; Fibroblasts/metabolism ; Fibrosis
Chemical Substances	Epoprostenol (DCR9Z582X0) ; Prostaglandins I
Language	English
Publishing date	2023-12-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.0000000000000286
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Article ; Online: Novel avenues for drug discovery in diabetic kidney disease.

Breyer, Matthew D / Kretzler, Matthias

Expert opinion on drug discovery

2017 , Page(s) 1–10

Abstract: Introduction: Diabetic kidney disease (DKD) has emerged as major cause of morbidity and mortality. After progressing to renal failure, over 70% of DKD patients are dead with five years. New treatments to slow this progression are desperately needed. ... ...

Abstract	Introduction: Diabetic kidney disease (DKD) has emerged as major cause of morbidity and mortality. After progressing to renal failure, over 70% of DKD patients are dead with five years. New treatments to slow this progression are desperately needed. Areas covered: This review highlights the current treatment options for people with DKD with a particular focus on angiotensin pathway blockade and the potential use of sodium glucose linked transporter 2 (SGLT2) inhibitors. These treatments are associated with an initial decrease in glomerular filtration rate (GFR) and albuminuria; there is also attention on renal hyperfiltration as therapeutic target. Both clinical and preclinical testing are facilitated by leveraging albuminuria reduction as a dynamic biomarker of drug effect linked to renal failure. It is critical to ensure that animal models exhibit both albuminuria and progressive loss of renal function so drug effects can be established in both. Expert opinion: New pathways and potential drug targets are emerging from gene expression profiling of human kidney biopsies and genome wide association studies. By harmonizing animal experimentation endpoints with clinical outcomes, focusing on disease pathophysiology and incorporating novel gene expression and biomarker changes, therapeutics can be advanced into clinical testing with greater confidence.
Language	English
Publishing date	2017-11-16
Publishing country	England
Document type	Journal Article
ZDB-ID	2259618-5
ISSN	1746-045X ; 1746-0441
ISSN (online)	1746-045X
ISSN	1746-0441
DOI	10.1080/17460441.2018.1398731
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Article ; Online: Drug discovery for diabetic nephropathy: trying the leap from mouse to man.

Breyer, Matthew D

Seminars in nephrology

2012 Volume 32, Issue 5, Page(s) 445–451

Abstract: Diabetic nephropathy is the single major cause of kidney failure in the industrialized world and given the emerging global pandemic of diabetes mellitus, its prevalence is expected to only increase. Because of the lack of dynamic biomarkers that define ... ...

Abstract	Diabetic nephropathy is the single major cause of kidney failure in the industrialized world and given the emerging global pandemic of diabetes mellitus, its prevalence is expected to only increase. Because of the lack of dynamic biomarkers that define the rate of kidney function loss, there are few proof-of-concept clinical trials for new therapeutics to treat diabetic nephropathy. A molecular understanding of the pathogenesis of diabetic nephropathy also is lacking. These deficiencies are magnified by the fact that most mouse models of diabetic nephropathy fail to show progressive kidney disease. Recently, some mouse models that showed requisite phenotypic changes of diabetic nephropathy have been identified. Validation of results obtained in these experimental models, and showing whether they accurately can predict clinical response to therapeutics in human diabetic nephropathy, must now be established.
MeSH term(s)	Animals ; Biomarkers, Pharmacological ; Clinical Trials as Topic ; Diabetic Nephropathies/drug therapy ; Diabetic Nephropathies/pathology ; Diabetic Nephropathies/physiopathology ; Disease Models, Animal ; Disease Progression ; Drug Discovery ; Humans ; Mice
Chemical Substances	Biomarkers, Pharmacological
Language	English
Publishing date	2012-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	604652-6
ISSN	1558-4488 ; 0270-9295
ISSN (online)	1558-4488
ISSN	0270-9295
DOI	10.1016/j.semnephrol.2012.07.007
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Article ; Online: Translating experimental diabetic nephropathy studies from mice to men.

Breyer, Matthew D

Contributions to nephrology

2011 Volume 170, Page(s) 156–164

Abstract: The laboratory mouse is among the best characterized and flexible experimental platforms available for the study of diabetic nephropathy (DN). However, studies of progressive kidney disease in mice have underscored several important technical ... ...

Abstract	The laboratory mouse is among the best characterized and flexible experimental platforms available for the study of diabetic nephropathy (DN). However, studies of progressive kidney disease in mice have underscored several important technical considerations for accurate phenotyping of renal function. Most mouse models of DN fail to exhibit progressive kidney disease. However, a few models have proved particularly useful. Despite the utility of these models, whether they can accurately predict clinical benefit of therapeutics in human DN remains to be established.
MeSH term(s)	Albuminuria/etiology ; Animals ; Diabetic Nephropathies/etiology ; Disease Models, Animal ; Glomerular Filtration Rate ; Humans ; Kidney/pathology ; Mice
Language	English
Publishing date	2011-06-09
Publishing country	Switzerland
Document type	Journal Article
ISSN	1662-2782 ; 0302-5144
ISSN (online)	1662-2782
ISSN	0302-5144
DOI	10.1159/000325651
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Article ; Online: Progress in progression?

Breyer, Matthew D

Journal of the American Society of Nephrology : JASN

2010 Volume 21, Issue 9, Page(s) 1414–1416

MeSH term(s)	Animals ; Diabetic Nephropathies/etiology ; Disease Progression ; Glomerular Filtration Rate ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Obese
Language	English
Publishing date	2010-09
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.2010070744
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