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Dr. Abais-Battad’s research mainly focuses on the interplay between the gut microbiota and the immune system as mediators of salt-sensitive hypertension and kidney disease, with a specific interest in how these pathways differ between males and females.

The main goal of Belin de Chantemele’s laboratory is to analyze the mechanisms whereby metabolic disorders such as obesity, diabetes and lipodystrophy, lead to cardiovascular disease. More specifically, they are interested in determining the contribution of leptin, a hormone secreted by the adipose tissue, to vascular disease and hypertension. A major focus of the lab is to understand the sex-specificity of the mechanisms leading to cardiovascular disease in obesity and diabetes and to understand how metabolic disorders abrogate the protective effects of female sex hormones.  All experiments are conducted in close collaboration with physicians and involve an integrative approach consisting of a wide range of physiological, pharmacological and molecular methods, and involving genetically engineered mouse models of disease.

    

Dr. Brands works in the field of cardiovascular-renal integrative physiology and hypertension. The longstanding interest is the renal and hormonal mechanisms for chronic blood pressure and circulatory system control in states of insulin resistance, hyperinsulinemia, and diabetes. His new work reveals a chronic sodium-retaining action of insulin, and shows that the sustained natriuresis and diuresis in uncontrolled Type I diabetes is due to the loss of insulin rather than hyperglycemia per se.

   

The interests of Dr. Chen’s lab include understanding the mechanism of nephron hypertrophy, which is implicated in setting the stage for progressive nephron damage. Dr. Chen’s lab is also interested in the cellular and molecular mechanisms underlying the nephron damage seen in acute kidney injury (AKI) and chronic kidney disease (CKD). Recent exciting novel observations made by Dr. Chen have motivated the Chen lab to also study novel insights into the pathogenesis of diabetic kidney disease and hypertension. The overall goal of the Chen lab is to identify potential molecular targets for the development of preventive and/or therapeutic strategies to preserve functional nephrons, prevent kidney failure, and maintain normal blood pressure.

   

Dr. Dong is a molecular geneticist and cardiologist with interests in elucidating the pathogenesis of obesity, diabetes, and hypertension by combined genetic, physiological, and clinical approaches.  His team performs cross-sectional, longitudinal, and interventional studies in the general population, community setting, and patients with clinical conditions.  A focus of his research is on vitamin D deficiency regarding epigenetics, cellular aging, inflammation, cardiometabolic disease, supplemental dosing and nutritional recommendation. 

   

The long-term goal of Dr. Dong’s laboratory is to delineate the mechanism of cell injury and death, its protection, and subsequent regeneration during kidney injury and kidney repair. Their current work is focused on mitochondria, metabolism, autophagy, and epigenetic regulation in acute and chronic kidney diseases. Thus far, they have published more than 400 full-length articles that have been cited for over 50,000 times with a Google Scholar H-index of 111, attesting their contribution to the field of kidney injury and repair in renal diseases and, cell stress response in general.

   

Dr. Fan’s lab uses multidisciplinary approaches with an array of techniques to investigate how genetic-based microvascular dysfunction in aging, hypertension, diabetes and obesity contributes to end-organ damage, including vascular cognitive impairment, Alzheimer's disease and Alzheimer's disease-related dementias (AD/ADRD), and renal disease. The lab also focuses on studying the contribution of changes in the actin cytoskeleton in vascular cells to the hemodynamics in cerebral and renal circulation, as well as changes in the actin cytoskeleton in podocytes in glomerular function. Recent work from the lab revealed that inhibition of sodium-glucose co-transporter 2 (SGLT2) and soluble epoxide hydrolase (sEH) reversed impaired cerebral hemodynamics and cognitive deficits. Ultimately, our goals are to develop novel biomarkers and new therapeutic strategies to prevent the onset, ensure early diagnosis and delay the progression of devastating cardiorenal and cerebral vascular diseases.

Dr. El-Marakby has a broad background in Physiology and Pharmacology with specific training and expertise in exploring the mechanisms regulating blood pressure and renal function in experimental animal models of cardio-metabolic disease. Recently, his research has focused on identifying the role of immune cells in halting the progression of renal vascular injury in hypertensive and diabetic animal models. His findings suggest that shifting macrophages and T cells polarization toward anti-inflammatory profiles is a key determinant in slowing the progression of renal vascular injury in cardio-metabolic disease. Utilizing in vitro and in vivo approaches to address the impact of hypertension and/or diabetes on renal and vascular function, he has published 70 manuscripts on this topic. His current research focus in exploring role of immune cells in the sexual dimorphism in obesity-induced renal vascular injury utilizing genetic and diet-induced models of obesity.

Studies in the Faulkner laboratory explore the mechanisms of high blood pressure, vascular damage and fetal growth restriction in obese and lean pregnancy. In particular, the laboratory focuses on the physiological alterations to the vasculature caused by abnormal hormone release and activity in the vasculature, placenta, adrenal gland and adipose tissue utilizing human tissues/cell lines and rodent models of preeclampsia. The laboratory is primarily exploring mechanisms of metabolic dysfunction, vascular endothelial cell biology and function, uterine artery blood flow, steroid hormone synthesis, placental hypoxia and inflammation. Studies are approached with a translational perspective, utilizing transgenic and surgical mouse models of preeclampsia as well as human tissues/cell lines to determine pathways involved in hypertension, vascular damage and fetal growth restriction in the context of pregnancy. These results lead to mechanistic exploration of the underlying biochemical, molecular and genetic factors involved. Experiments to test our hypotheses include functional measures of blood pressure and vascular function, protein and mRNA expression measures as well as hormone, cell signaling and genetic analyses, among others.

   

Dr. Harris is a clinical vascular and exercise physiologist.  Using pharmacological and non-pharmacological interventions that are coupled with state-of-the-art invasive and non-invasive methodologies, his research aims to understand the mechanisms of vascular endothelial dysfunction in a variety of patient populations.

   

The research in Ilatovskaya lab is aimed at advancing our understanding of the mechanisms that underlie kidney disease and renal blood pressure control. The laboratory specializes in investigating the regulation of mitochondrial bioenergetics in the different aspects of renal disorders, with a major focus on salt-sensitivity and sex differences in pathobiology. The lab uses in vivo, ex vivo and in vitro techniques to study physiology with a multi-pronged approaches at the molecular, cellular, and whole-body levels. The lab employs many unique methods, such as single-channel electrophysiology, the state-of-the-art imaging, measurements of mitochondrial bioenergetics, chronic telemetry studies, and other sophisticated techniques. 

   

Dr. James primary emphasis is the investigation of mechanisms of kidney disease caused by common, yet complex traits. A key focus has been on the interaction between hypertension and hyperglycemia in the progression of kidney disease.  He hopes to further his research with studies to decipher mechanistic aspects of acute and chronic kidney disease including the role of o-glycosylation (O-GlcNAcylation) in hypertension, vascular complications and kidney disease. 

   

Research in Dr. Kriegel Lab is broadly focused on understanding how alterations in microRNAs (miRNAs), protein coding genes, and metabolites influence cardiovascular disease, cardiorenal syndrome, and renal disease. They utilize discovery-based approaches to studying these complex problems by blending next-generation technologies with molecular biology techniques, systems physiology, classical physiological studies, and translational research. Their current work is focused in three main areas: 1) determining mechanisms regulating declining renal function in hypertension, diabetes and CKD, 2) determining mechanisms regulating cardiovascular dysfunction in cardiorenal syndrome and during cancer treatment, and 3) understanding fundamental sex differences in renal and cardiovascular physiology and pathophysiology.  

Research in the Kwon lab relates to the fundamental principles of extracellular vesicle biology and applications of extracellular vesicles in the kidney. The Kwon lab currently probes their biogenesis and contribution to acute kidney injury and chronic kidney disease. 

As a basic-translational researcher, Dr. Lokeshwar’s research programs are focused on benign and malignant diseases of the bladder, kidney and prostate with an emphasis on developing biomarkers and targeted treatments.

   

Dr. Long’s lab is mainly interested in the molecular underpinnings of vascular smooth muscle (VSMC) phenotypic plasticity, which underlies a variety of prominent vascular diseases. Her expertise relates to the utilization of RNA/DNA deep sequencing, bioinformatics, molecular biology, and translational vascular disease models (arterial venous fistula, wire injury, and aortic aneurysm) to discover and dissect novel regulators in different vascular disorders. She has a long-standing interest in regulation of novel long noncoding RNAs (lncRNAs) and coding genes in vascular smooth muscle pathophysiology.

   

The main goal of Dr. Lucas’s laboratory is to better characterize the protective role of the epithelial sodium channel (ENaC) in protecting glomerular endothelial and pulmonary capillary endothelial barrier function in the context of inflammatory disease, including glomerulonephritis, diabetes and ARDS. They have developed a TNF-derived peptide that directly activates ENaC in both epithelium and endothelium and they are currently evaluating its therapeutic potential in animal models (glomerulonephritis, diabetes) and (in case of ARDS) in phase 2 clinical trials.

     

Hydromineral homeostasis is intimately tied to blood pressure control and its disruption leads to renal and cardiovascular diseases. Hypertension and chronic kidney diseases continue to take one of the highest tolls on human health despite considerable advances in biomedical research. Dr. Mamenko’s long-term scientific interest is to study cellular cascades and end-effectors, such as ion channels and membrane receptors, contributing to the maintenance of water-electrolyte balance. Their experimental arsenal includes direct monitoring of ion channel activity with patch-clamp electrophysiology in combination with fluorescence/confocal microscopy, biochemical and molecular biology approaches. The expertise allows performing the experiments both in cultured cells and in a native tissue.

   

Dr. Manicassamy’s work focuses on understanding the molecular mechanisms by which innate immune cells shape adaptive immune responses, and harnessing such mechanisms to treat immune cell-mediated inflammatory diseases including acute kidney diseases and in the design of novel vaccines against pathogens and tumors.

   

Studies in the Mattson laboratory examine the normal and pathophysiological regulation of renal function and arterial blood pressure. A particular emphasis is placed on the paracrine, autocrine, and hormonal regulation of renal tubular and vascular function. Additional studies are geared toward an understanding of the genetic basis of hypertension and renal disease. The work performed in his laboratory utilizes techniques taken from molecular biology, biochemistry, immunology, and integrative physiology to address the role of the kidney in the regulation of sodium and water homeostasis and arterial pressure.

   

Dr. Mirza’s research interest involves immunosuppression, advanced organ preservation techniques, obesity surgery for transplant recipients and role of  biological agents in transplantation. He has extensively worked and published on reducing barriers to transplantation in obese patients suffering with end stage renal disease requiring dialysis. 

Dr. Mohamed’s research interest is to understand pathophysiology of kidney diseases (AKI, AKI-CKD nexus and PKD) and hypertension in male and females and elucidate cellular and molecular mechanisms using a broad range of biochemical, cellular, immunological, molecular biology techniques and whole animal physiology. In-depth, he is keenly interested in the characterization of signaling pathways and the identification of therapeutic targets by utilizing in vitro cell culture and clinically relevant preclinical animal models.

Dr. Mulloy’s research interests include clinical investigation of immunosuppressive therapies for renal transplantation, and hypertension in chronic kidney disease. She is the Co-PI for the NIH sponsored SPRINT protocol for evaluation blood pressure in patients with chronic kidney disease.

Dr. O’Connor’s laboratory studies the role of red blood cell vascular congestion in acute kidney injury as well as the mechanisms underlying the protective effects of alkali therapy to slow glomerular filtration rate decline in chronic kidney disease.

   

Dr. Sullivan is a recognized expert and leader in the field of sex differences in cardiovascular and renal physiology and pathophysiology. Ongoing studies in the laboratory are focused on 1) sex differences in AKI and the impact of AKI on pregnancy outcomes; 2) mechanisms of T cell activation and the role of T cells in blood pressure (BP) control; 3) enhanced susceptibility of females to high-fat diet induced cardiovascular disease. Her work has been continuously funded by the NIH and the American Heart Association since becoming a tenure track faculty member in 2008. Dr. Sullivan is also an exceptional educator and mentor, with a demonstrated commitment to the training of the next generation of scientists. 

   

Research in Dr. Thangaraju’s laboratory is divided into two interrelated areas of interest. The first project is to understand the role of GPR109A, a receptor for Niacin, a vitamin B3, and small-chain fatty acid Butyrate, in cancer prevention and treatment. They found that GPR109A expression significantly reduced human breast and colon cancer and Gpr109a deficiency is associated with increased tumor growth and metastasis which leads to reduced overall survival. They applied this research strategy to understand the role of GPR109A in the regulation of polycystic kidney disease (PKD). GPR109A activation reduces cAMP by inhibiting Adenylyl Cyclase (AC), which leads to inhibition of growth-promoting signaling. It has been well established that increased cAMP and deregulated intracellular calcium levels are the prognostic factors for ADPKD cystogenesis. Therefore, they are studying the role of GPR109A in the prevention and treatment of ADPKD cystogenesis. 

   

Dr. Wang is a genetic epidemiologist. Her research mainly focuses on population studies to elucidate the role of genetic factors and their interactions with environmental factors in the occurrence of diseases, particularly cardiovascular diseases, obesity and hypertension. 

   

Dr. Wei’s research is mainly focused on the epigenetic regulation mechanisms in kidney injury, including both acute kidney injury (AKI) and chronic kidney diseases (CKD).  Currently they are examining the pro-injurious role of a long non-coding RNA (lncRNA) GSTM3P1 (an RNA transcript from pseudogene) in ischemic AKI, its interaction with microRNA-668, and its regulation to the parent gene GSTM3.  In addition, they are exploring various lncRNAs in other AKI models (cisplatin nephrotoxicity, sepsis) and CKD models to understand their role in renal cell death, renal repair, and fibrosis.

Dr. Zhu’s research has focused on: Cellular aging, epigenetic aging and aging prevention: Clinical and population research to identify and elucidate how environmental factors (i.e.: stress, maternal nutrition) and lifestyle factors (nutrition, physical activity) impact the molecular aging process. Sodium-gut-heart and brain health: using RCT design and omics approaches (microRNA, metabolomics, SCFA profiling and shotgun metagenomics sequencing) to study the underlying mechanisms of salt-sensitive hypertension, as well as sodium-gut-heart, and sodium-gut-brain connections. Promote digital (mobile) technology to aide blood pressure (BP) management in minority, underserved populations (community outreach): To develop tailored home BP monitoring, BP text messaging programs in underserved minority populations.