RESEARCH INTERESTS
Cardiovascular Development and Disease Biology Lab
I have almost 20 years of research experience in the field of cellular and molecular biology. Primary focus of my research work is to investigate the mechanisms leading to the development of cardiac hypertrophy, fibrosis and vascular inflammation in the context of disease states like atherosclerosis, myocardial injury and diabetes. The overall objective of our research is to provide the foundation for novel therapies directed at the treatment of a broad spectrum of cardiovascular disorders (CVDs). Following are the research areas that are currently being investigated in my laboratory:
- Reactivation of Developmental Gene Program following Cardiac Injury in Adult
Adult heart has limited regenerative capacity therefore it will be invaluable to create an environment to reinitiate cardiomyocyte proliferation and/or to inhibit the profibrotic/apoptosis pathway in the context of adult cardiac injuries for keeping the cell viable and able to perform normal physiological function. Therefore, identification of the novel signaling pathways that may directly enhance the protective responses of cardiomyocyte against detrimental pathways will be invaluable for restoration of homeostasis in the milieu of cardiac injury. Our lab is currently investigating the consequences of reactivation of developmental gene program following cardiac injury in adult with implications in normal cardiac repair/regeneration mechanisms in near future.
- Unfolded Protein Response (UPR) and Cardiovascular Disorders: A tilt towards Pro-survival and Cellular Homeostasis
The research is focused in examining the involvement of ER stress and associated signalling pathway in the development of diabetic cardiomyopathy. ER stress is steered initially at compensating for any damage but a prolonged damage can eventually trigger apoptosis. The question remains what are the regulatory mechanisms of ER by which cell either decide to resume cellular homeostasis or to undergo apoptosis in the context of different cardiac injuries.
- Senescence-induced Inflammation in Vascular Calcification (VC)
Senescence-induced inflammation may contribute to the development of chronic diseases associated with aging, like VC, CVDs. Administration of senolytic drug removes only senescent cells through apoptosis but it has no effect on inflammation. Hence research should explore different ways to break this vicious cycle to eliminate senescent cells and inhibit inflammation, with the goal of mitigating VC. Research is undergoing to identify the molecular players involved in augmenting senescence and inflammation could be harnessed for the management and treatment of not only VC but for other age related disease. The effect of targeting both senescence and inflammation by combinatorial application of anti-inflammatory and senolytic drugs to attenuate VC is being investigated.
- Particulate Matter (PM) -induced Damage in Vascular and Cardiac Tissues
The mechanisms involving Particulate matter (PM10 and PM 2.5) induced CVDs are not much worked upon as most researches are based on epidemiology and cohort analysis. Even though everyone is subjected to air pollution, the changes that happen with age may worsen the health effects of PM in older individuals. Compromised individuals (like aging) are more susceptible to the adverse effects of PM in developing conditions like arrhythmia, hypertension, myocardial infarction, atherosclerosis, heart failure and ischaemic heart diseases. So, the question lies that, how does PM influence the hallmarks of aging, such as inflammation, oxidative stress and senescence in older adults? Experiments are undergoing to delineate the molecular mechanisms associated with the development of PM-induced damage in vascular and cardiac tissues.
Academic:
PhD. (2002-2007): Department of Zoology, Miami University, Oxford, Ohio, USA
M.Sc.(1997-1999): Zoology with specialization in Endocrinology, Ballygunge Science College, University of Calcutta, India
B.Sc. (1994-1997): Zoology, Ladu Brabourne College, University of Calcutta, India
Post-PhD Experience:
Postdoctoral Research Fellow (2007-2011): Cincinnati Children’s Hospital Medical Center, USA
Postdoctoral Research Associates (2011-2013) :Cincinnati Children’s Hospital Medical Center, USA
DBT Bio-CARe Women Scientist (2015-16): Dept. of Genetics, University of Calcutta, India
UGC-Assistant Professor (2016-2026): Dept. of Life science & Biotechnolgy, Jadavpur University, Kolkata, India
Associate Professor (2026-Present): Institute of Health Sciences (IHS), Presidency University, Kolkata, India
I did my doctoral studies from Miami University, Oxford, Ohio and obtained a postdoctoral fellowship in Dr. Katherine Yutzey’s laboratory at Cincinnati Children’s Hospital Medical Centre (CCHMC), Ohio, USA. After returning to India I joined the department of Genetics, CU as DBT-Women Scientist in 2015 to start my research career in India. Then I moved to Jadavpur University as an UGC-Assistant Professor and established my own independent research laboratory. After spending almost 10 years at Jadavpur University I have joined the Institute of Health Sciences (IHS), Presidency University, Kolkata as Associate Professor to continue my research journey. Currently, my laboratory is using different cell/molecular biology tools to understand the regulation of different cardiac transcription factors during cardiac development and diseases. My group has been funded through the support from DBT, UGC, DST-SERB, ANRF, CSIR, WBDSTBT.
POSTDOCTORAL RESEARCH TRAINING AND EXPERIENCE (2007-April 2013):
I obtained a postdoctoral fellowship in Dr. Katherine Yutzey’s laboratory at Cincinnati Children’s Hospital Medical Center (CCHMC), Ohio, USA. I studied the function of Forkhead Box O (FoxO) transcription factor in heart development and disease. During my postdoctoral training I secured independent funding from American Heart Association (AHA), USA and published papers in peer-reviewed journals including, JBC, Circulation Research, JMCC, Developmental Biology.
Summary:
- I identified FoxO transcription factor as one of the critical factor in promoting autophagy in cardiomyocytes (Sengupta A. et.al, Journal of Biological Chemistry 284(41):28319-31, 2009).
- I also identified that FoxO transcription factors promote cardiomyocytes survival upon induction of oxidative stress in neonatal cultured cardiomyocytes and also in adult heart during ischemic injury in mice in vivo (Sengupta A. et.al, Journal of Biological Chemistry 286(9):7468-7478, 2011).
- I demonstrated that FoxO1 is required in endothelial but not myocardial cell lineages during cardiovascular development (Sengupta A. et.al, Development and Dynamics 241(4):803-13; 2012).
- My studies also extend to better understand the molecular mechanism of inhibition of proliferation and promotion of cell cycle withdrawal in cardiomyocytes during neonatal period and in adult heart (Sengupta, A. et.al, Circulation Research, 112(2):267-277, 2013).
- I also examined the ability of Tbx20 to promote post-natal and adult cardiomyocyte proliferation in mice with cardiomyocyte-specific Tbx20 gain-of-function beginning in the fetal period (Chakraborty S., Sengupta A and Yutzey Katherine, Journal of Molecular and Cellular Cardiology, 62:203-213, 2013).
- Internal Examiner/Expert/reviewer in the department of Life Science & Biotechnology, JU
- BOS Member of Department of Environmental Science, Mizoram University, Mizoram
- External Examiner/Expert/reviewer:
Department of Biochemistry, University of Calcutta
Department of Microbiology, University of Kalyani
Department of Microbiology, West Bengal State University
Department of Lifesciences, Presidency University
- Meeting Organized: Seved as a co-organiser in the Regional Young Investigator Meeting (RYIM), Kolkata, Biswa Bangla Convention Centre, Kolkata, 6th-8th December, 2023
- Refresher Course Organized (UGC-HRDC, JU): Served as aco-organiser in the "Emerging areas in Life Sciences", Department of Life Science and Biotechnology, Jadavpur UniversityJan 27th — Feb 8th, 2020
- Editorial Board member of the journal “Scientific Reports”
·
Teaching Experiences:
My teaching philosophy has been shaped in part through my experiences with great teachers who have positively influenced me during my education. My dissertation advisor and my postdoc mentor have been instrumental in leading me through many lessons both in science and life. These teachers acted as facilitators who helped not only to shape my education but also led me to a greater understanding of the scientific process and enhanced my desire for a career in biomedical research. I aspire to be like them and to give back the same level of respect, patience, and encouragement to my students (both as a teaching instructor and research mentor).
Through my experiences as a teacher, I have developed my own teaching style that continually builds upon my education and allows me to be an effective instructor. My strengths as a teacher include:
1) My enthusiasm for science. I like to share my respect for science with students by bringing theoretical points to the level of their everyday experiences. I demonstrate that the ideas and concepts we cover in class are not at all abstract and that they have real application in the world and in their lives. The association of science with personal life experiences helps the students develop their own respect for science and often my enthusiasm for the subject is spread to them.
2) My ability to relate to the students. I enjoy getting to know my students, learning about their aspirations, and helping them achieve their goals. Some students are auditory learners and absorb more by hearing the ideas spoken aloud, while others are visual learners and prefer to see things written down. Some prefer to learn by discussing smaller, individual concepts first, and gradually constructing a detailed picture of a larger concept; while others prefer to understand the overall concept first, to give them a foundation on which to place new facts. My variety of teaching experiences has helped me greatly improve my ability to read a class, realize when a specific method of presentation is not working, and modify it to be more effective.
3) My capability to communicate science. I think science should be clarified in a way that makes it fascinating and not overly complex. I believe that I have a keen ability to convey complicated information in a simplified way that helps students see through obscure information and really understand the concept, which provides a foundation of knowledge that can be expanded in advanced classes. By presenting material in terms of the students' everyday experiences and curiosities, complex ideas can become more interesting to them and therefore the students are much more willing to put forth the effort required for them to understand the concepts thoroughly.
A) Teaching Assistantship during my doctoral tenure
During my PhD tenure at Miami University, Oxford, Ohio (USA) I taught several courses as a teaching assistant, which includes:
- General microbiology
- Experiments with microbes
- Biological concepts: Ecology, evolution and genetics
- Biological concepts: Structure, function, cellular and molecular biology
- Developmental Biology.
B) Teaching responsibilities as UGC-Assistant Professor in the Dept of Life Science & Biotechnology, Jadavpur University
For the past ten (2016-2016) years in Jadavpur University I have followed the same ideas of teaching and try to incorporate all the new information pertaining to the subject each year to enhanced the quality of my teaching. I want my students to understand that the ideas and concepts we cover in class are not at all abstract and that they have real application in the world and in their lives. The association of science with personal life experiences helps the students develop their own respect for science and often my enthusiasm for the subject is spread to them. My more than 20 years of research experience in the field of cellular and molecular biology of cardiovascular diseases is a great addition to the master degree students in terms of knowing the details pathophysiological aspects of cardio-pulmonary diseases. As I’m a cardiac developmental biologist by training I have introduced a new course as “Animal Developmental Biotechnology” in the Masters curriculum in the department for Life Science & Biotechnology at Jadavpur University. My overall goal towards my student is to motivate them to think critically in a way that help them to build their career as a good teacher as well as good research mentor for next generation.
· Courses taught at Jadavpur University:
Theory
- Cell Biology
- Animal Developmental Biotechnology
- Recombinant DNA Technology
Practical
Cell Biology Laboratory:
- Cell Viability assay and determination of proliferation indices in cultured mammalian cell.
- Immunohistochemistry of tissue section.
- Examination of chicken embryo at different developmental stages in presence of stress.
PhD Awarded from Jadavpur University
1. Name: Jayeeta Samanta
Title of thesis: Forkhead Transcription Factor Functions in Stress-Induced Cardiomyocyte Hypertrophy and Calcification
Year in which awarded: 2022
2. Name: Arunima Mondal
Title of thesis: The Role of Development Regulatory Factors YAP1 and FOXM1 and Associated Molecular Signaling in the Induction of Cardiomyocyte Hypertrophy and Fibrosis in Rodent Diabetic Cardiomyopathy Model
Year in which awarded: 2024
3. Name: Shreya Das
Title of thesis: The interplay of cardiac developmental factors T-box transcription factors 20 (Tbx20) and bone morphogenetic protein 2 (Bmp2) and their cross-talk with miR-101-3p in regulating cardiac homeostasis in rodent cardiomyopathy model.
Year in which awarded: 2025
Registered PhD Student: Madhuchhanda Das
PUBLICATIONS:
1. Das S, Das M, Chakraborty S, Arunima Sengupta. MiR-101-3p Promotes Cardiac Senescence and Inflammation via Targeting Tbx20 and Bmp2 to Perturb Cardiac Homeostasis. J Cell Physiol. Dec;240(12):e70122 (2025).
2. S. Mukherjee, S. Das, S. Gupta, S.P. Hui, Arunima Sengupta and A. Ghosh. Pyruvate plus uridine augments mitochondrial respiration and prevents cardiac hypertrophy in zebrafish and H9c2 cells. J. Cell Sci. 138 (9), jcs263653. (2025).
3. A Mondal, S Das, M Das, S Chakraborty, Arunima Sengupta. YAP1-mediated dysregulation of ACE-ACE2 activity augments cardiac fibrosis upon induction of hyperglycemic stress. Biochimica et Biophysica Acta (BBA)-General Subjects, 1868(9):130666 (2024)
4. Shreya Das, Arunima Mondal, Chandrani Dey, Santanu Chakraborty, Rudranil Bhowmik, Sanmoy Karmakar and Arunima Sengupta. ER stress induces upregulation of transcription factor Tbx20 and downstream Bmp2 signaling to promote cardiomyocyte survival. Journal of Biological Chemistry 299(4):103031 (2023)
5. Arunima Mondal, Shreya Das, Jayeeta Samanta, Santanu Chakraborty and Arunima Sengupta. Yap induces hyperglycemic stress-mediated cardiac hypertrophy and fibrosis in an AKT-FOXM1 dependent signaling pathway. Archives of biochemistry & Biophysics;722: 109198 (2022)
6. Shreya Das, Arunima Mondal, Jayeeta Samanta, Santanu Chakraborty and Arunima Sengupta. Unfolded protein response during cardiovascular disorders: a tilt towards prosurvival and cellular homeostasis. Molecular & Cellular Biochemistry 476:4061-4080. (2021)
7. Samanta J, Mondal A, Saha S, Chakraborty S, Arunima Sengupta. Induction of cardiomyocyte calcification is dependent on FoxO1/NFATc3/ Runx2 signaling. In vitro Cellular & Developmental Biology, Animal 57:973-986. (2021)
8. Samanta J, Mondal A, Saha S, Chakraborty S, Arunima Sengupta. Oleic acid protects from arsenic induced cardiac hypertrophy via AMPK/FoxO/NFATc3 pathway. Cardiovascular Toxicology 20(3):261-280 (2020)
9. Arunima sengupta, Vladimir Kalinichenko, Katherine E Yutzey. FoxO and FoxM1 transcription factors have antagonistic functions in neonatal cardiomyocyte cell cycle withdrawal and IGF1 gene regulation. Circulation Research. 112(2):267-27 (2013).
10. Santanu Chakraborty, Arunima Sengupta, Katherine E Yutzey. Tbx20 promotes cardiomyocyte proliferation and persistence of fetal characteristics in adult mouse hearts. Journal of Molecular and Cellular Cardiology. 62: 203-13 (2013).
11. Arunima Sengupta, Santanu Chakraborty, Jihye Paik, Katherine E. Yutzey, Heather J. Evans-Anderson. FoxO1 is required in endothelial but not myocardial cell lineages during cardiovascular development. Development and Dynamics, 241(4):803-13 (2012).
12. Arunima Sengupta, Jeffery D. Molkentin, Ji-Hye Paik, Ronald A. DePinho and Katherine E. Yutzey. FoxO Transcription Factors Promote Cardiomyocyte Survival Upon Induction of Oxidative Stress. Journal of Biological Chemistry, 286(9):7468-7478 (2011).
13. Arunima Sengupta, Molkentin JD, Yutzey KE. FoxO transcription factors promote autophagy in cardiomyocytes. Journal of Biological Chemistry. 284(41): 28319-31 (2009).
BOOK CHAPTERS:
1. Advances in Experimental Medicines & Biology, Vol. 1358, Oxidative Stress and Toxicity in Reproductive Biology and Medicine; ISBN 978-3-030-89339-2, Editors: Kavindra Kumar Kesari and Shubhadeep Roychoudhury. Tale of viruses in male infertility (Chapter 13) (Springer Nature Switzerland AG 2022)
2. Exploring Medical Biotechnology – In Vivo, In Vitro, In Silico Biotechnology from Labs to Clinics and Basic to Advanced, ISBN: 978-1-032-29555-8, DOI: 10.1201/9781003302131. Book Chapter 20: RNA Interference (RNAi) : A Boon to Medical Biotechnology
3. Exploring Medical Biotechnology – In Vivo, In Vitro, In Silico Biotechnology from Labs to Clinics and Basic to Advanced, ISBN: 978-1-032-29555-8, DOI: 10.1201/9781003302131, Book Chapter 07: CRISPR-Cas9, Molecular Scissors in Medical Biotechnology
Presidency University Students Corner