Ira Tabas
Columbia University in the City of New York
H-index: 131
North America-United States
Description
Ira Tabas, With an exceptional h-index of 131 and a recent h-index of 76 (since 2020), a distinguished researcher at Columbia University in the City of New York, specializes in the field of Cadiometabolic disease.
His recent articles reflect a diverse array of research interests and contributions to the field:
Ihh as a biomarker and therapeutic target for nonalcoholic steatohepatitis (nash)
Loss of TIM4-Dependent Efferocytosis in Kupffer Cells Promotes Liver Fibrosis in Nonalcoholic Steatohepatitis
Efferocytosis-induced lactate enables the proliferation of pro-resolving macrophages to mediate tissue repair
A therapeutically targetable TAZ-TEAD2 pathway drives the growth of hepatocellular carcinoma via ANLN and KIF23
BRCC3-Mediated NLRP3 Deubiquitylation Promotes Inflammasome Activation and Atherosclerosis in Tet2 Clonal Hematopoiesis
Circulating indian hedgehog is a marker of the hepatocyte-TAZ pathway in experimental NASH and is elevated in humans with NASH
Efferocytosis in liver disease
PFKFB2-mediated glycolysis promotes lactate-driven continual efferocytosis by macrophages
Professor Information
University | Columbia University in the City of New York |
---|---|
Position | Columbia University Medical Center |
Citations(all) | 72206 |
Citations(since 2020) | 28696 |
Cited By | 54640 |
hIndex(all) | 131 |
hIndex(since 2020) | 76 |
i10Index(all) | 267 |
i10Index(since 2020) | 193 |
University Profile Page | Columbia University in the City of New York |
Research & Interests List
Cadiometabolic disease
Top articles of Ira Tabas
Ihh as a biomarker and therapeutic target for nonalcoholic steatohepatitis (nash)
2023-06-13 Assigned to THE TRUSTEES OF COLUMBIA UNIVERSITY IN THE CITY OF NEW YORK reassignment THE TRUSTEES OF COLUMBIA UNIVERSITY IN THE CITY OF NEW YORK ASSIGNMENT OF ASSIGNORS INTEREST (SEE DOCUMENT FOR DETAILS). Assignors: TABAS, IRA, WANG, XIAOBO
Published Date
2024/2/8
Loss of TIM4-Dependent Efferocytosis in Kupffer Cells Promotes Liver Fibrosis in Nonalcoholic Steatohepatitis
Background and aims Hepatocyte apoptosis is a key feature of non-alcoholic steatohepatitis (NASH), but the fate of apoptotic hepatocytes in NASH is poorly understood. Herein we explore the hypothesis that impaired TIM4-mediated clearance of dead hepatocytes by liver macrophages (efferocytosis) is impaired in NASH and drives the progression to liver fibrosis. Methods Kupffer cell (KC)-TIM4 expression and efferocytosis were assayed in normal and NASH liver from humans and diet-induced NASH mice. The engulfment of human and mouse apoptotic hepatocytes by primary human and mouse liver KCs was assayed ex vivo. Causation was assessed in NASH mice using anti-TIM4 antibodies, KC-TIM4-knockout, or inducible KC-TIM4 expression, with analyses focused on efferocytosis of apoptotic hepatocytes by liver macrophages and liver fibrosis. Results In human and mouse NASH liver, apoptotic hepatocytes accumulated and was associated with the loss of the KC efferocytosis receptor TIM4. Anti-TIM4 inhibited the engulfment of apoptotic hepatocytes by primary human and mouse liver KCs ex vivo, and anti-TIM4 administration to early NASH mice worsened liver macrophage efferocytosis and accelerated the progression to fibrotic NASH. A similar result was obtained by genetically deleting TIM4 in KCs in NASH mice. Most importantly, genetic restoration of macrophage TIM4 in NASH mice enhanced the clearance of apoptotic hepatocytes by liver macrophages and decreased liver fibrosis. Conclusions The loss of macrophage TIM4 that occurs during NASH progression impairs the clearance of apoptotic hepatocytes by liver …
Authors
Hongxue Shi,Xiaobo Wang,Brennan Gerlach,Arif Yurdagul Jr,Mary Moore,Faridoddin Mirshahi,Luisa Ronzoni,Arun Sanyal,Luca Valenti,Chyuan-Sheng Lin,Ira Tabas
Journal
bioRxiv
Published Date
2024
Efferocytosis-induced lactate enables the proliferation of pro-resolving macrophages to mediate tissue repair
The clearance of apoptotic cells by macrophages (efferocytosis) prevents necrosis and inflammation and activates pro-resolving pathways, including continual efferocytosis. A key resolution process in vivo is efferocytosis-induced macrophage proliferation (EIMP), in which apoptotic cell-derived nucleotides trigger Myc-mediated proliferation of pro-resolving macrophages. Here we show that EIMP requires a second input that is integrated with cellular metabolism, notably efferocytosis-induced lactate production. Lactate signalling via GPR132 promotes Myc protein stabilization and subsequent macrophage proliferation. This mechanism is validated in vivo using a mouse model of dexamethasone-induced thymocyte apoptosis, which elevates apoptotic cell burden and requires efferocytosis to prevent inflammation and necrosis. Thus, EIMP, a key process in tissue resolution, requires inputs from two independent …
Authors
David Ngai,Maaike Schilperoort,Ira Tabas
Journal
Nature Metabolism
Published Date
2023/12
A therapeutically targetable TAZ-TEAD2 pathway drives the growth of hepatocellular carcinoma via ANLN and KIF23
Background & AimsDespite recent progress, long-term survival remains low for hepatocellular carcinoma (HCC). The most effective HCC therapies target the tumor immune microenvironment (TIME), and there are almost no therapies that directly target tumor cells. Here, we investigated the regulation and function of tumor cell-expressed Yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ) in HCC.MethodsHCC was induced in mice by Sleeping Beauty-mediated expression of MET, CTNNB1-S45Y, or TAZ-S89A, or by diethylnitrosamine plus CCl4. Hepatocellular TAZ and YAP were deleted in floxed mice via adeno-associated virus serotype 8-mediated expression of Cre. TAZ target genes were identified from RNA sequencing, confirmed by chromatin immunoprecipitation, and evaluated in a clustered regularly interspaced short palindromic repeats interference (CRISPRi) screen …
Authors
Yoshinobu Saito,Dingzi Yin,Naoto Kubota,Xiaobo Wang,Aveline Filliol,Helen Remotti,Ajay Nair,Ladan Fazlollahi,Yujin Hoshida,Ira Tabas,Kirk J Wangensteen,Robert F Schwabe
Journal
Gastroenterology
Published Date
2023/6/1
BRCC3-Mediated NLRP3 Deubiquitylation Promotes Inflammasome Activation and Atherosclerosis in Tet2 Clonal Hematopoiesis
BACKGROUND Clonal hematopoiesis (CH) has emerged as an independent risk factor for atherosclerotic cardiovascular disease, with activation of macrophage inflammasomes as a potential underlying mechanism. The NLRP3 (NLR family pyrin domain containing 3) inflammasome has a key role in promoting atherosclerosis in mouse models of Tet2 CH, whereas inhibition of the inflammasome product interleukin-1β appeared to particularly benefit patients with TET2 CH in CANTOS (Cardiovascular Risk Reduction Study [Reduction in Recurrent Major CV Disease Events]). TET2 is an epigenetic modifier that decreases promoter methylation. However, the mechanisms underlying macrophage NLRP3 inflammasome activation in TET2 (Tet methylcytosine dioxygenase 2) deficiency and potential links with epigenetic modifications are poorly understood. METHODS We used cholesterol-loaded TET2-deficient …
Authors
Mustafa Yalcinkaya,Wenli Liu,Leigh-Anne Thomas,Malgorzata Olszewska,Tong Xiao,Sandra Abramowicz,Eirini P Papapetrou,Marit Westerterp,Nan Wang,Ira Tabas,Alan R Tall
Journal
Circulation
Published Date
2023/11/28
Circulating indian hedgehog is a marker of the hepatocyte-TAZ pathway in experimental NASH and is elevated in humans with NASH
Background & AimsNon-alcoholic steatohepatitis (NASH)-induced liver fibrosis is emerging as the most common cause of liver disease. For evaluation of therapies, there is a pressing need to identify non-invasive, mechanism-based biomarkers. A pro-fibrotic process relevant to human NASH involves a pathway in which a transcriptional regulator called TAZ (WWTR1) in hepatocytes induces the secretion of pro-fibrotic Indian hedgehog (IHH). We therefore reasoned that circulating IHH may be a useful mechanism-based marker to assess changes in NASH fibrosis.MethodsCirculating IHH was assessed in wild-type and hepatocyte-TAZ-silenced NASH mice and in three separate cohorts of patients with mild–moderate NASH.ResultsCirculating IHH was elevated in mice with diet-induced NASH compared with chow-fed mice or with NASH mice in which hepatocyte TAZ was silenced, which is an effective means to …
Authors
Mary Patricia Moore,Xiaobo Wang,Hongxue Shi,Marica Meroni,Alessandro Cherubini,Luisa Ronzoni,Elizabeth J Parks,Jamal A Ibdah,R Scott Rector,Luca Valenti,Paola Dongiovanni,Ira Tabas
Journal
JHEP Reports
Published Date
2023/5/1
Efferocytosis in liver disease
The process of dead cell clearance by phagocytic cells, called efferocytosis, prevents inflammatory cell necrosis and promotes resolution and repair. Defective efferocytosis contributes to the progression of numerous diseases in which cell death prominent, including liver disease. Many gaps remain in our understanding how liver macrophages carry out efferocytosis and how this process goes awry in various types of liver diseases. Studies thus far have suggested that, upon liver injury, liver resident Kupffer cells (KCs) and infiltrating monocyte-derived macrophages (MoMϕs) clear dead cells, limit inflammation, and, through macrophage reprogramming, repair liver damage. However, in unusual settings, efferocytosis can promote liver disease. In this review, we will focus on efferocytosis in various types of acute and chronic liver diseases, including metabolic dysfunction-associated steatohepatitis. Understanding the …
Authors
Hongxue Shi,Mary P Moore,Xiaobo Wang,Ira Tabas
Published Date
2023/11/16
PFKFB2-mediated glycolysis promotes lactate-driven continual efferocytosis by macrophages
Resolving-type macrophages prevent chronic inflammation by clearing apoptotic cells through efferocytosis. These macrophages are thought to rely mainly on oxidative phosphorylation, but emerging evidence suggests a possible link between efferocytosis and glycolysis. To gain further insight into this issue, we investigated molecular–cellular mechanisms involved in efferocytosis-induced macrophage glycolysis and its consequences. We found that efferocytosis promotes a transient increase in macrophage glycolysis that is dependent on rapid activation of the enzyme 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 2 (PFKFB2), which distinguishes this process from glycolysis in pro-inflammatory macrophages. Mice transplanted with activation-defective PFKFB2 bone marrow and then subjected to dexamethasone-induced thymocyte apoptosis exhibit impaired thymic efferocytosis, increased thymic …
Authors
Maaike Schilperoort,David Ngai,Marina Katerelos,David A Power,Ira Tabas
Journal
Nature metabolism
Published Date
2023/3
Professor FAQs
What is Ira Tabas's h-index at Columbia University in the City of New York?
The h-index of Ira Tabas has been 76 since 2020 and 131 in total.
What are Ira Tabas's top articles?
The articles with the titles of
Ihh as a biomarker and therapeutic target for nonalcoholic steatohepatitis (nash)
Loss of TIM4-Dependent Efferocytosis in Kupffer Cells Promotes Liver Fibrosis in Nonalcoholic Steatohepatitis
Efferocytosis-induced lactate enables the proliferation of pro-resolving macrophages to mediate tissue repair
A therapeutically targetable TAZ-TEAD2 pathway drives the growth of hepatocellular carcinoma via ANLN and KIF23
BRCC3-Mediated NLRP3 Deubiquitylation Promotes Inflammasome Activation and Atherosclerosis in Tet2 Clonal Hematopoiesis
Circulating indian hedgehog is a marker of the hepatocyte-TAZ pathway in experimental NASH and is elevated in humans with NASH
Efferocytosis in liver disease
PFKFB2-mediated glycolysis promotes lactate-driven continual efferocytosis by macrophages
...
are the top articles of Ira Tabas at Columbia University in the City of New York.
What are Ira Tabas's research interests?
The research interests of Ira Tabas are: Cadiometabolic disease
What is Ira Tabas's total number of citations?
Ira Tabas has 72,206 citations in total.