Katarzyna Anna Cieslik, Ph.D.
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Positions
- Associate Professor
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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
- Cieslik KA, Trial J, Crawford JR, Taffet GE, Entman ML. "Adverse fibrosis in the aging heart depends on signaling between myeloid and mesenchymal cells; role of inflammatory fibroblasts.." J Mol Cell Cardiol. 2014;70:56-63. Pubmed PMID: 24184998
- Cieslik KA, Trial J, Entman ML. "Mesenchymal stem cell-derived inflammatory fibroblasts promote monocyte transition into myeloid fibroblasts via an IL-6-dependent mechanism in the aging mouse heart.." FASEB Journal. 2015;29:3160-3170. Pubmed PMID: 25888601
- Trial J, Heredia CP, Taffet GE, Entman ML, Cieslik KA. "Dissecting the role of myeloid and mesenchymal fibroblasts in age-dependent cardiac fibrosis.." Basic Res Cardiol. 2017;112(4):34. Pubmed PMID: 28478479
- Cieslik KA, Sekhar RV, Granillo A, Reddy A, Medrano G, Heredia CP, Entman ML, Hamilton DJ, Li S, Reineke E, Gupte AA, Zhang A, Taffet GE. "Improved cardiovascular function in old mice after N-Acetyle Cystein and Glycine supplemented diet: Inflammation and mitochondrial factors.." J Gerontol A Biol Sci Med Sci. 2018;73:1167-1177. Pubmed PMID: 29538624
- Trial J, Diaz Lankenau R, Angelini A, Tovar Perez JE, Taffet GE, Entman ML, Cieslik KA. "Treatment with a DC-SIGN ligand reduces macrophage polarization and diastolic dysfunction in the aging female but not male mouse heart.." Geroscience. 2021;43:881-899. Pubmed PMID: 32851570
- Angelini A, Trial J, Ortiz-Urbina J, Cieslik K. "Mechanosensing dysregulation in the fibroblast, a hallmark of the aging heart." Ageing Research Reviews. 2020;63:101150. Pubmed PMID: 32846223
- Angelini A, Ortiz-Urbina J, Trial J, Reddy AK, Malovannaya A, Jain A, Entman ML, Taffet GE, Cieslik KA. "Sex-specific phenotypes in the aging mouse heart and consequences for chronic fibrosis.." Am J Physiol Heart Circ Physiol.. 2022 Aug 1;323(2):H285-H300. Pubmed PMID: 35714177
Memberships
- American Heart Association
- Member (01/2008)
- Society for Leukocyte Biology
- (01/2015)
- The American Association of Immunologists
- (01/2015)
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