Email

cieslik@bcm.edu

Positions

Associate Professor

Medicine-Cardiovascular Sciences
Baylor College of Medicine
Houston, TX US

Addresses

Office (Office)

Neurosensory Building
3rd Floor, Room N308A
Houston, TX 77030
United States
Phone: (713) 798-8375

Education

PhD from Jagiellonian University

Krakow, Poland

MSc from Jagiellonian University

Krakow, Poland

Postdoctoral Training at UT- Health Science Center at Houston

Houston, Texas United States

Postdoctoral Training at Baylor College of Medicine

Houston, Texas United States

Honors & Awards

Cardiac Contractility, Hypertrophy and Failure Study Section, Standing Member

National Institutes of Health (01/2020 - 12/2024)

Cardiac Contractility, Hypertrophy and Failure Study Section, Ad hoc

National Institutes of Health (01/2020)

Fellow

American Heart Association (06/2019)

Cardiac Contractility, Hypertrophy and Failure Study Section, Ad hoc

National Institutes of Health (01/2018)

NIEHS Travel Award - 7th Annual Winter Eicosanoid Conference

Baltimore, MD (03/2005)

Professional Interests

• cardiac aging
• fibrosis
• inflammation

Professional Statement

Advances in modern medicine extend the human lifespan, but with an increasing number of aging people, medical care is facing new challenges. Heart failure with preserved ejection fraction (HFpEF) is nearly exclusively found in older patients. HFpEF is characterized by abnormal diastolic function, which is caused by an increase in the stiffness of the heart's left ventricle and a decrease in left ventricular relaxation.
Dr. Cieslik's research interests focus on the dysregulation of cardiac fibroblasts and immune cells in the aging heart that may lead to diastolic dysfunction.
The primary extracellular matrix (ECM)-producing cells in the heart are fibroblasts. ECM provides not only a scaffold for cells, but its structure can affect cell phenotype and function. In the aged heart, ECM composition and architecture is altered. To determine the effect of matrix on fibroblasts' function, the lab cultures them in 2D and 3D settings and examines how decellularized matrices from the aged hearts can affect young fibroblast phenotype and vice versa.
Dr. Cieslik's lab also examines the role of various macrophages, dendritic cells, and lymphocytes in the activation of cardiac fibroblasts leading to subsequent fibrosis. In addition, her lab applies various treatments that modulate either fibroblasts or immune cell phenotypes to characterize the molecular and cellular signalings involved in the inflammatory responses in young versus old animals.
Finally, the lab studies not only the differences in young versus old mice but also how sex affects the phenotype of the studied cells or the heart function, which is also observed in the human population.

Websites

Selected Publications

• Cieslik KA, Taffet GE, Carlson S, Hermosillo J, Trial J, Entman ML "Immune-inflammatory dysregulation modulates the incidence of progressive fibrosis and diastolic stiffness in the aging heart.." J. Mol. Cell. Cardiol.. 2011 Jan;50(1):248-56. Pubmed PMID: 20974150
• Cieslik KA, Trial J, Entman ML "Defective Myofibroblast Formation from Mesenchymal Stem Cells in the Aging Murine Heart Rescue by Activation of the AMPK Pathway.." Am. J. Pathol.. 2011 Oct;179(4):1792-806. Pubmed PMID: 21819956
• Cieslik KA, Trial J, Carlson S, Taffet GE, Entman ML "Aberrant differentiation of fibroblast progenitors contributes to fibrosis in the aged murine heart: role of elevated circulating insulin levels.." FASEB J.. 2013 Apr;27(4):1761-71. Pubmed PMID: 23303205
• Cieslik KA, Taffet GE, Crawford JR, Trial J, Mejia Osuna P, Entman ML. "AICAR-dependent AMPK activation improves scar formation in the aged heart in a murine model of reperfused myocardial infarction." J Mol Cell Cardiol. 2013;63:26-36. Pubmed PMID: 23871790

Memberships

American Heart Association

Member (01/2008)

Society for Leukocyte Biology

(01/2015)

The American Association of Immunologists

(01/2015)