Alison Kriegel, PhD

Alison Kriegel, PhD

Associate Professor


  • Physiology

Contact Information


PhD, Physiology, Medical College of Wisconsin, 2008

Research Experience

  • Cardiovascular Physiological Phenomena
  • Cell Communication
  • Cell Physiological Phenomena
  • Hypertension
  • MicroRNA
  • Molecular Biology
  • Paracrine Communication
  • Physiological Genomics
  • Renal Physiology

Methodologies and Techniques

  • miRNA analysis
  • Models of Cardiac Pathology
  • Models of Renal Pathology
  • Next-generation RNA Sequencing
  • qRT-PCR
  • RNA analysis
  • Rodent Echocardiography
  • Rodent Left Ventricle Pressure-Volume Loop Analysis
  • Western Blot

Research Interests

Cardiovascular Physiology  |  Genetics and Genomics  |  Molecular and Cellular Physiology  |  Renal Physiology

Our research is broadly centered on understanding how alterations in microRNAs and protein coding genes influence cardiovascular disease, renal disease, and cardiorenal syndromes. Cardiorenal syndromes are a grouping of human clinical conditions where primary disease in either the heart or the kidney contributes to the development of secondary disease in the other organ.

Our current focus is on cardiorenal syndrome type 4 (CRS4), also known as chronic renocardiac syndrome, a condition in which chronic kidney disease (CKD) contributes to the development of cardiovascular diseases including hypertrophy, diastolic dysfunction, reduction in cardiac function and increased risk of cardiovascular events.

CRS4 is clinical problem that has received a great deal of attention in recent years because of the large number of people impacted and the high associated healthcare costs. In 2010 the Centers for Disease Control estimated that more than 10% of adults in the United States population chronic kidney disease, and cardiovascular pathology is leading cause of death in these patients. Treatment of CRS4 remains challenging because so little is understood about the pathology of the disease. Adult patients with CKD often have age associated comorbidities, such as diabetes, hypertension, and atherosclerosis, making it difficult to identifying mediators of the pathology in this population.

Cardiorenal Syndrome Type 4

Our goals are focused on identifying the essential components of cardiorenal syndromes and their therapeutic targets. We have started to investigate the molecular mediators of this conditions using a 5/6 nephrectomy (5/6 NX) model of CKD in Sprague Dawley rats. This model of CKD allows us to study CRS4 related pathologies in the absence of confounding comorbidities that would independently impact the heart, such as atherosclerosis, diabetes and hypertension.

Our current goals in CRS4 research interest include:

  • Identifying pathways involved with CRS4 disease progression
  • Understanding miRNA regulation of pathways involved with pathological LV remodeling and dysfunction in a rat model of CKD
  • Circulating factors in CKD that contribute to the development of CRS4
  • We combine in vivo approaches for studying cardiac and renal function with advanced molecular techniques to comprehensively study the factors that influence left ventricular pathology. Frequently utilized techniques in our laboratory include: echocardiography, left ventricle pressure-volume relationship analysis, chronic and acute blood pressure recordings, cell culture models (siRNA, miRNA), in vitro and in vivo miRNA suppression, immunohistochemistry, in situ hybridization, western blot analysis, ELISA, miRNA and mRNA next generation sequencing and qRT-PCR.

    Research for this project is supported an American Heart Association Scientist Development Grant (13SDG17100095).

    Supporting documents:

    Supplemental Table 1 (XLSX)
    Supplemental Table 3 (XLSX)
    Supplemental Table 4 (XLSX)

    Students with an interest in this research are encouraged to contact Dr. Kriegel at