About

Jonathan P. Katz, MD, is an Associate Professor of Medicine (Gastroenterology) at the University of Pennsylvania Perelman School of Medicine. His research broadly focuses on the functional analyses of gastrointestinal epithelial proliferation, differentiation, and carcinogenesis, utilizing both in vivo and in vitro approaches, including murine models and innovative three-dimensional tissue culture systems. His work aims to dissect the critical pathways regulating gastrointestinal epithelial homeostasis and disease, with particular emphasis on the roles of transcriptional regulators in the Krüppel-like factor (KLF) family, specifically KLF4 and KLF5, especially in the context of the esophagus. Dr. Katz's investigations include exploring the interactions between KLF4 and WNT5A, as well as between KLF5 and the tumor suppressor p53, to understand how these factors control the balance between proliferation and differentiation in gastrointestinal epithelia and how this balance is disrupted during mucosal injury and carcinogenesis. He holds several leadership roles, including Director of the Undergraduate Student Scholars Program at the University of Pennsylvania Perelman School of Medicine, and directs the Molecular Pathology and Imaging Core at the NIH Center for Molecular Studies in Digestive and Liver Diseases. His contributions extend to participating in multiple research and clinical collaborations within the university's cancer center, regenerative medicine institute, and translational medicine programs.

Research topics

• Cancer research
• Biology
• Cell biology
• Medicine
• Chemistry

Selected publications

• CMGH Reviews: From Comprehensive Narratives to Concise Insights

  Cellular and Molecular Gastroenterology and Hepatology · 2025-01-01

  editorialOpen accessSenior author

  Review articles have been a mainstay of CMGH since our first issue in 2015, serving to synthesize, consolidate, and disseminate essential knowledge on topics related to the cellular and molecular biology of the gastrointestinal system. Reviews published in our journal strive to provide a coherent and comprehensive narrative that highlights both connections and disagreements within a field. These papers should define current knowledge and understanding within an area and identify critical gaps. They promote rigor through a critical assessment of the methods, results, and conclusions across a body of literature.

  PublisherOA PDFDOI

• The Evolution of CMGH as The Basic Research Journal in Gastroenterology and Hepatology: “H” is for “Home”

  Cellular and Molecular Gastroenterology and Hepatology · 2025-01-01

  editorialOpen access1st authorCorresponding

  In 2015, the American Gastroenterological Association launched a new journal, Cellular and Molecular Gastroenterology and Hepatology (CMGH), as a dedicated platform for basic, mechanistic research in gastrointestinal and liver biology. Although some grew concerned that the National Institutes of Health might be shifting toward a focus on translational research, Dr Francis Collins, Director of the National Institutes of Health, stated clearly that “basic research is the engine that powers tomorrow’s therapeutic discoveries.”1 As articulated in its inaugural editorial, “CMGH is the answer to the looming question of where, within the realm of gastroenterology- and hepatology-related journals, to publish high-quality, laboratory-focused research.

  PublisherOA PDFDOI

• Krüppel-like Factors in the Gastrointestinal Tract

  Cells · 2025-09-28

  reviewOpen accessSenior authorCorresponding

  -like factors (KLFs) are a family of transcriptional regulators that play crucial roles in regulating diverse cellular processes including development, proliferation, differentiation, metabolism, and carcinogenesis across various tissues. KLFs play pivotal roles in gastrointestinal pathologies, and exhibit tissue- and cell-type-specific expression patterns throughout the gastrointestinal tract. During gastrointestinal (GI) development, KLFs orchestrate the transition from embryonic to adult gene programming, with specific family members being essential for proper organogenesis and tissue formation. KLFs also function as context-dependent modulators of GI homeostasis, inflammation, and carcinogenesis in adult tissues and interact with major signaling pathways such as PI3K/AKT, NF-κB, Wnt, Notch, MAPK, and TGF-β. This review comprehensively examines the roles of KLFs in GI health and disease, focusing on their expression patterns, regulatory mechanisms, function in normal homeostasis, and therapeutic implications for gastrointestinal disorders.

  PublisherOA PDFDOI

• Rapid Research, High Impact: CMGH’s Short-Form Initiative

  Cellular and Molecular Gastroenterology and Hepatology · 2025-01-01

  editorialOpen accessSenior author

  The mission of CMGH since its inception in 2015 is to publish hypothesis-driven, mechanistically novel research spanning gastroenterology, hepatology, and pancreatology. Fundamental discoveries across cell biology, immunology, physiology, microbiology, genetics, and neurobiology of the gastrointestinal (GI) system are mainly communicated through the Original Article format. These full-length original research articles comprehensively report mechanisms underlying normal cell, tissue, and organ function and pathobiology.

  PublisherOA PDFDOI

• Guiding Principles: A New Article Type to Promote Rigor, Reproducibility, and Transparency

  Cellular and Molecular Gastroenterology and Hepatology · 2025-09-03

  editorialOpen access

  Technologies and approaches in gastrointestinal research are emerging and evolving rapidly, yet clear consensus on best practices for these methods often lags. Such ambiguity can compromise rigor, reproducibility, and transparency, risking meaningful advancements. Therefore, CMGH is excited to introduce Guiding Principles, a new article format to support scientific consistency and veracity by tackling research ‘gray areas.’ Guiding Principles articles will delineate a framework that the gastrointestinal research community can apply to complex experimental paradigms, such as key experimental and analytical considerations and reporting standards.

  PublisherOA PDFDOI

• Sa1183 KLF5 INHIBITION ALTERS MMP EXPRESSION AND PODOSOME FORMATION IN ESOPHAGEAL SQUAMOUS EPITHELIAL CELLS

  Gastroenterology · 2024-05-01

  articleSenior author
  PublisherDOI

• KLF5 inhibition initiates epithelial-mesenchymal transition in non-transformed human squamous epithelial cells

  Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · 2024-06-22 · 5 citations

  articleOpen accessSenior authorCorresponding
  PublisherOA PDFDOI

• CMGH: Evolving to Advance Gastroenterology and Hepatology Research

  Cellular and Molecular Gastroenterology and Hepatology · 2024-01-01

  editorialOpen accessSenior author

  S ince its inaugural issue in 2015, Cellular and Mo- lecular Gastroenterology and Hepatology (CMGH) has expertly delivered an open-access platform for highquality, innovative, and impactful laboratory-focused research in the fields of gastroenterology and hepatology.As we lead CMGH into its second decade, we are committed to maintaining the journal's focus on mechanistic and translational gastrointestinal (GI) research, promoting rigor and reproducibility, and providing a fair, rapid, and transparent review process.The prior Editors-in-Chief, Drs Jerrold Turner, Klaus Kaestner, and Michael Pack, grew CMGH to be the go-to journal for the gastrointestinal, liver, and pancreas research communities, particularly for studies grounded in basic science.We understand that we have big shoes to fill, but with a dynamic and broad-based Board of Editors (Drs Brian DeBosch, Nan Gao, Kathryn Hamilton, Frdric Lemaigre, Guang Sheng Ling, and Gisa Tiegs), we will ensure that CMGH remains the preeminent journal focused on highimpact, mechanistic GI and hepatology basic science research.Publishing in CMGH assures authors that the research communities most connected to and essential to their field will read their work.We recognize that the world of science and publishing is changing, and opportunities need to exist for rapid dissemination of findings and commentary on findings in real-time.As we take on the leadership of CMGH, we will work to improve the journal's reach and engagement with authors and readers, including by growing its social media presence through Dr Lindsey Kennedy, the journal's Social Media Editor.We look forward to interacting with the GI research community.For example, we will hold meet-the-editor events at key GI research conferences-we enjoyed meeting many of you at Digestive Disease Week in Washington, DC.In addition, we are launching new initiatives and adding special topics editors who will cover themes relating to professional development, mentoring, and diversity, equity, and inclusion.We will seek to expand our presence, not only in the United States but throughout the world.Teams from diverse backgrounds are more innovative, creative, and productive, and we will seek input from individuals at various career levels and from groups underrepresented in science and medicine.There will be challenges and opportunities in the next 5 years.Publication costs can be a major obstacle for many authors, and we are proud that CMGH costs, especially for American Gastroenterological Association members, are much lower than many of our peer open-access journals.We will strive to maintain a quick turnaround from submission to publication while upholding a rigorous and transparent review process.We want to lead the way by publishing new research guidelines, similar to those for clinical journals, and enhancing the rigor and reproducibility of submissions, including recognizing the challenges posed by AI.Although AI presents certain threats, we also see opportunities for AI in science and publishing, and we will work with our publisher to take advantage of these.There are many facets to consider as we work to advance CMGH, to improve its impact, and to prepare for the challenges ahead.We are excited for the support of the GI research community in these endeavors and look forward to the next 5 years!

  PublisherOA PDFDOI

• KLF5 and p53 comprise an incoherent feed-forward loop directing cell-fate decisions following stress

  Cell Death and Disease · 2023-05-02 · 9 citations

  articleOpen accessSenior authorCorresponding

  In response to stress, cells make a critical decision to arrest or undergo apoptosis, mediated in large part by the tumor suppressor p53. Yet the mechanisms of these cell fate decisions remain largely unknown, particularly in normal cells. Here, we define an incoherent feed-forward loop in non-transformed human squamous epithelial cells involving p53 and the zinc-finger transcription factor KLF5 that dictates responses to differing levels of cellular stress from UV irradiation or oxidative stress. In normal unstressed human squamous epithelial cells, KLF5 complexes with SIN3A and HDAC2 repress TP53, allowing cells to proliferate. With moderate stress, this complex is disrupted, and TP53 is induced; KLF5 then acts as a molecular switch for p53 function by transactivating AKT1 and AKT3, which direct cells toward survival. By contrast, severe stress results in KLF5 loss, such that AKT1 and AKT3 are not induced, and cells preferentially undergo apoptosis. Thus, in human squamous epithelial cells, KLF5 gates the response to UV or oxidative stress to determine the p53 output of growth arrest or apoptosis.

  PublisherOA PDFDOI

• Neutrophils in Cancer and Potential Therapeutic Strategies using Neutrophil-derived Exosomes

  Preprints.org · 2023-04-25 · 12 citations

  preprintOpen access

  Neutrophils are the most abundant immune cells and make up about 70% of white blood cells in human blood and play a critical role as the first line of defense in the innate immune response. They also help regulate the inflammatory environment to promote tissue repair. However, in cancer, neutrophils can be manipulated by tumors to either promote or hinder tumor growth depending on the cytokine pool. Studies have shown that tumor-bearing mice have increased levels of neutrophils in peripheral circulation, and that neutrophil-derived exosomes can deliver various cargos, including lncRNA and miRNA, which contribute to tumor growth and degradation of extracellular matrix. Exosomes derived from immune cells generally possess anti-tumor activities and induce tumor-cell apoptosis by delivering cytotoxic proteins, ROS generation, H2O2 or activation of Fas-mediated apoptosis in target cells. Engineered exosome-like nanovesicles have been developed to deliver chemotherapeutic drugs precisely to tumor cells. However, tumor-derived exosomes can aggravate cancer-associated thrombosis through the formation of neutrophil extracellular traps. Despite the advancements in neutrophil-related research, a detailed understanding of tumor-neutrophil crosstalk is still lacking and remains a major barrier in developing neutrophil-based or targeted therapy. This review will focus on the communication pathways between tumors and neutrophils, and the role of neutrophil-derived exosomes (NDEs) in tumor growth. Additionally, potential strategies to manipulate NDEs for therapeutic purposes will be discussed.

  PublisherOA PDFDOI

Recent grants

• NIH Grant R21DK073888

  NIH · $429k · 2009

• NIH Grant K08DK002809

  NIH · $647k · 2004

• Mechanisms of Esophageal Carcinogenesis

  NIH · $48.5M · 2003–2024

• Training Program in Gastrointestinal Sciences

  NIH · $13.8M · 1975–2025

• NIH Grant R03DK062850

  NIH · $159k · 2005

Frequent coauthors

• Klaus H. Kaestner

  University of Pennsylvania

  33 shared

• Marie–Pier Tétreault

  31 shared

• Yizeng Yang

  University of Pennsylvania

  27 shared

• Abha Goyal

  23 shared

• Noel Victor

  23 shared

• Janelle Billig

  23 shared

• Yizeng Yang

  22 shared

• Hiroshi Nakagawa

  Cleveland Clinic

  22 shared

Labs

• Katz LaboratoryPI