Tabas Lab
Location and Contact Information
- Lab 212-305-5669
- Office 212-305-9430
Principal Investigator
The Tabas laboratory studies the cellular biology of cardiometabolic disease, with an emphasis on the molecular-cellular mechanisms of advanced atherosclerosis and hepatic insulin resistance and NASH in obesity, and the links between these processes.
The studies on advanced atherosclerosis have focused on integrated processes that combine to promote advanced plaque progression, with a focus on defective clearance of apoptotic cells (efferocytosis) and impaired inflammation resolution. In the efferocytosis field, current studies are focused on (a) cell biological pathways triggered by macrophage metabolism of ingested and degraded apoptotic cells, particularly pathways related to inflammation resolution; and (b) linking macrophages processes that promote atherosclerosis progression to both human genetic risk factors for coronary artery disease, i.e., polymorphisms that regulate specific genes, as well as systemic insulin resistance. The inflammation resolution project has a strong focus on processes that promote plaque regression and on the therapeutic potential of promoting resolution, e.g., through the use of atherosclerosis-targeted nanoparticles packaged with resolution mediators. Additionally, an exciting new area in the lab involves identifying specific mechanistic links between impaired resolution pathways and clonal hematopoiesis of indeterminate potential (CHIP), which is a major risk factor for atherosclerosis and coronary artery disease in humans over the age of 60.
The lab's studies on hepatic insulin resistance, which is an important driver of atherosclerosis, led to the discovery of a new calcium-stimulated pathway in hepatocytes that plays a key role in glucagon-mediated excessive glucose production, insulin resistance, fatty liver, dyslipidemia, impaired thrombolysis, and adipose tissue inflammation in the setting of obesity and type 2 diabetes. Ongoing studies are investigating (a) how the pathway may promote atherosclerotic plaque progression by affecting plaque macrophages; and (b) strategies to translate our discoveries into new types of drugs to treat type 2 diabetes and prevent diabetes-driven atherosclerotic plaque progression.
Related to the lab's metabolism work, we study hepatocyte pathways in non-alcoholic steatohepatitis (NASH), with current investigations focused on (a) the role of a transcription factor called TAZ in both NASH fibrosis and NASH-associated hepatocellular carcinoma; (b) new mechanistic insight into known human genetic risk factors for NASH fibrosis; and (c) new therapeutic strategies to prevent steatosis-to-NASH progression based on our findings.
The overall approach of the laboratory is to elucidate in-depth mechanisms using molecular-cell biological approaches; test causation in normal physiology and disease models using genetically engineered mice; probe relevance to humans through the study of normal and diseased human tissues and human genetics; and conceive and test novel and mechanism-based therapies in the cardiometabolic arena. Our human genetics studies are being conducted in collaboration with the CUMC Cardiovascular and Metabolic Precision Medicine Program, led by Dr. Muredach Reilly, and include plans to study human iPSC-derived macrophages that can be genetically engineered using CRISPR/Cas9 to mimic or "correct" disease-causing human mutations. We also have collaborations with Dr. Danish Saleheen at Columbia, who directs a translational program studying humans who have heterozygous and homozygous null mutations in thousands of individual genes.
The laboratory's philosophy is one of collaboration, not competition, and emphasis is placed on long-term, in-depth, and rigorous studies. Dr. Tabas places great emphasis on mentoring, particularly fostering independence and career guidance. His trainees have had great success in career development grants from the NIH (K99/R00) and American Heart Association and subsequently with NIH R01 grants soon after leaving the lab for independent tenure-track Assistant Professorships at major university research organizations.
Lab Members
Lale Ozcan
- Faculty Consultant for Lab
Dr. Lale Ozcan received her medical degree from Istanbul University Cerrahpasa School of Medicine and did a postdoctoral work at Harvard University focusing on mechanisms linking metabolic stress with insulin resistance. She then joined the laboratory of Dr. Ira Tabas at Columbia University where she studied the detailed signaling pathways and mechanisms underlying excessive glucose production and altered hepatic insulin signaling in obesity. Dr. Ozcan is currently a tenure-track Assistant Professor in the Department of Medicine at Columbia University and her work focuses on exploring novel signaling pathways that control metabolic homeostasis with the ultimate goal to provide new therapeutic options for metabolic diseases.
Saheli Chowdhury, PhD
Saheli completed her PhD at CSIR-Indian Institute of Chemical Biology, Kolkata, India. Her PhD thesis pivoted around understanding aspects of the ubiquitin-proteasome system in metabolism dysfunction-associated steatotic liver disease (MASLD) and hepatotoxicity. Before acquiring her PhD, she did an Integrated MSc in Biotechnology from St. Xavier’s College, Kolkata, India. Her present research in the Tabas lab focuses on unraveling the mechanisms linking metabolism dysfunction-associated steatohepatitis (MASH) to atherosclerosis.
Eui Jung Jung, DVM, PhD
Eui Jung (EJ) earned her D.V.M. degree from Seoul National University, South Korea in 2017. She went on to complete her Ph.D. in Biomedical Sciences at the same institution in 2024, where her research focused on the role of Arg/N-degron pathway-mediated autophagy in metabolic syndromes, including metabolic dysfunction-associated fatty liver disease and type 2 diabetes mellitus. In September 2024, EJ joined Dr. Tabas’s laboratory as a postdoctoral research scientist. Her current work investigates the role of efferocytosis in the regression of metabolic dysfunction-associated steatohepatitis (MASH), as well as how genetic loss of function of the phospholipid-remodeling enzyme MBOAT7 in hepatic stellate cells influences MASH progression.
Kleopatra Avrampou
Kleopatra attended the master's program of Molecular Biology-Biomedicine at the University of Crete & IMBB Institute in Greece and performed her master's thesis as a visiting student at Icahn School of Medicine in Mount Sinai. In 2021, she finished her Ph.D. obtained from the University of Crete, as a visiting grad student at Mount Sinai and NYU Langone Medical Center investigating the molecular and cellular mechanisms activated in response to systemic and cellular stress. In 2022, she joined Tabas's lab to explore macrophage metabolic pathways, cellular crosstalk, and cellular stress in atherosclerosis.
George Kuriakose
George is from Kerala, India. He received his B.Sc. in Biology from Kerala University and M.Sc. in Biology from Mahatma Gandhi University, Kerala. He came to U.S.A. in 1992 and started working in the Department of Ophthalmology, Columbia University as a Research Staff Associate. In 1997 he moved to the Tabas Lab as a Senior Research Worker. His primary responsibilities include (a) maintaining and breeding various transgenic and knockout mouse lines; (b) sectioning of OCT embedded and paraffin mouse tissue samples; (c) histological staining and immunohistochemical analysis; (d) quantitation and qualitative analysis of atherosclerotic lesions in aortic arch with computer-aided imaging systems; (e) isolating primary human and murine cells, and maintaining a wide variety of immortal cell lines; (f) PCR, Southern and Western analysis; (g) standard molecular biology techniques; (h) bone marrow transplantation in mouse; (i) extracting and purifying human, rabbit and mouse plasma lipoprotein (VLDL, LDL and HDL) by preparative ultra centrifugation; (j) isotopic labeling (14C, 3H, 125I) of various cholesterol and protein components of lipoproteins for studying lipoprotein trafficking via endocytic and selective uptake pathways; (k) TLC and FPLC; and (l) Protein purification by column chromatography.
David Ngai
David completed his PhD in the Department of Laboratory Medicine and Pathobiology at the University of Toronto, Canada, in 2021. For his thesis, he investigated the role of the collagen-binding receptor tyrosine kinase, Discoidin Domain Receptor-1 (DDR1), in vascular smooth muscle cell mechanosignaling and how this contributes to pathologies such as vascular calcification. He joined the Tabas lab in July 2021 to investigate how metabolites produced by shifts in macrophage metabolism during efferocytosis help to drive further apoptotic cell clearance and inflammation resolution.
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Santosh Reddy Sukka
Santosh received his Master’s degree in Pharmacology from JNTU-Hyderabad, India, in 2012. He then joined CSIR-Central Drug Research Institute, India as a research scholar. In January 2021, he completed his Ph.D. at the Department of Pharmacology of the CSIR-Central Drug Research Institute, India, where he explored novel immunometabolic mechanisms regulating cardiometabolic disorders. He joined the Tabas laboratory at Columbia University in March 2021 with an interest in how macrophages metabolize the cargo of engulfed and degraded apoptotic cells and how this metabolism affects macrophage biology relevant to the progression and regression of atherosclerosis besides macrophage cellular senescence, particularly in the area of plaque regression.
Xiaobo Wang
Xiaobo Wang received his PH.D. degree in 2008 from China Agricultural University in Beijing, China. After three years postdoctoral research working on the smooth muscle gene expression during smooth muscle cell phenotypic modulation in Albany Medical College, Xiaobo joined Dr. Tabas’ lab as a research scientist to focus on macrophage apoptosis during atherosclerosis.
