About

Ana Mora, MD, is a professor in the Department of Internal Medicine at Ohio State University College of Medicine, with a research focus on lung fibrosis, aging, and mitochondrial biology. She received her MD from Universidad Nacional de Colombia Medical School in Bogota, Colombia, and completed postdoctoral training as a Fellow in the Department of Microbiology and Immunology at Vanderbilt University. Her academic career includes faculty positions at Emory University in the Division of Pulmonary, Allergy and Critical Care Medicine and at the University of Pittsburgh, where she also served as Director of Education at the Aging Institute. Since February 2021, she has been part of the Division of Pulmonary Critical Care and Sleep Medicine at Ohio State University as Associate Director of Lung Research. Her research is centered on elucidating the pathogenic mechanisms involved in lung disrepair and fibrosis, with particular emphasis on how aging-related cell perturbations contribute to these processes. She pioneered aging studies demonstrating that vulnerability and persistence of ER stress responses are key components of age-related susceptibility to lung injury and fibrosis. Additionally, her work has elucidated the role of alterations in mitochondrial homeostasis in the pathogenesis of Idiopathic Pulmonary Fibrosis and identified it as a potential therapeutic target. Dr. Mora has published over 96 peer-reviewed articles, contributed to book chapters, and editorial comments. Her research has significantly advanced understanding of the cellular and molecular mechanisms underlying lung fibrosis and aging.

Research topics

• Genetics
• Biology
• Medicine
• Cell biology
• Pathology
• Internal medicine
• Computer Science
• Cancer research
• Immunology
• Computational biology
• Gerontology

Selected publications

• RNAseq (with probes) data from the lung (right) of a 58 year-old white male

  Cellular Senescence Network (SenNet) · 2026-02-17

  datasetOpen access
  PublisherDOI

• RNAseq (with probes) data from the lung (right) of a 24 year-old white male

  Cellular Senescence Network (SenNet) · 2026-02-17

  datasetOpen access
  PublisherDOI

• SpaFlow depicts the dynamics of ligand-receptor interaction in spatial transcriptomics data

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-04-21

  articleOpen access

  Abstract Spatial transcriptomics (ST) enables the study of cell-cell communication in native tissue context, but current methods for the ligand-receptor interaction (LRI) inference generally rely on static, distance-based assumptions. Here we present SpaFlow, a reaction-diffusion framework that models ligand diffusion, binding, dissociation, production and degradation to infer spatially resolved LRI activity and hotspots from ST data. Across paired 10x Visium and CosMx metastatic renal cell carcinoma datasets, SpaFlow outperformed existing methods in recovering spatially coherent LRIs, with inferred LRI activity showing stronger association with downstream signaling. In hepatocellular carcinoma after neoadjuvant immunotherapy, SpaFlow identified CXCL12-CXCR4 hotspots enriched at immune-rich tumor boundaries in responders. In aging mouse heart, SpaFlow resolved niche-specific pro-fibrotic and senescence-associated signaling, highlighting Postn-Itgav/Itgb5 as an additional pro-fibrotic axis and Angptl2-Pirb as a candidate mediator of inter-niche senescence-related communication. In human idiopathic pulmonary fibrosis lung, SpaFlow localized CXCL12-CXCR4 signaling between adventitial fibroblasts and CD4 T cells, CD8 T cells, and B cells in the fibrotic surrounding regions. Together, SpaFlow provides a physically informed framework for quantifying spatially constrained cell-cell communication and mechanistically interpreting signaling patterns in complex tissues.

  PublisherDOI

• RNAseq (with probes) data from the lung (right) of a 24 year-old white male

  Cellular Senescence Network (SenNet) · 2026-02-17

  datasetOpen access
  PublisherDOI

• RNAseq (with probes) data from the lung (right) of a 29 year-old white male

  Cellular Senescence Network (SenNet) · 2026-02-18

  datasetOpen access
  PublisherDOI

• RNAseq (with probes) data from the lung (left) of a 62 year-old white male

  Cellular Senescence Network (SenNet) · 2026-02-18

  datasetOpen access
  PublisherDOI

• RNAseq (with probes) data from the lung (left) of a 55 year-old white male

  Cellular Senescence Network (SenNet) · 2026-02-17

  datasetOpen access
  PublisherDOI

• RNAseq (with probes) data from the lung (right) of a 58 year-old white male

  Cellular Senescence Network (SenNet) · 2026-02-17

  datasetOpen access
  PublisherDOI

• Transcriptional and spatial profiling of fibroblasts from human lungs highlights CTHRC1+ cells as fibrogenic signaling hubs in fibrosis

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-04-10

  articleOpen access

  Lung fibroblasts are key regulators of tissue homeostasis and extracellular matrix (ECM) remodeling, and their aberrant activation drives the progressive parenchymal scarring characteristic of idiopathic pulmonary fibrosis (IPF), a fatal disease with limited therapeutic options. Despite their central pathogenic role, lung fibroblasts are difficult to isolate due to their embedded position within the ECM, and standard in vitro culture conditions may lead to the loss of their native functional and transcriptional characteristics, hampering the study of fibroblast behavior in disease. The transcriptional heterogeneity of lung fibroblast subtypes and the extent to which culture-induced alterations diverge from native tissue signatures remain poorly understood. Here, we integrated single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics of lung tissue from IPF patients and age-matched healthy donors with transcriptomic profiling of cultured fibroblasts collected at passages 1 and 6 after isolation using three optimized protocols: whole lung cell suspension (WLCS), negative fraction enrichment, and outgrowth. Tissue-based analysis identified six transcriptionally distinct mesenchymal subtypes: alveolar, adventitial, inflammatory, peribronchial, CTHRC1+ and smooth muscle cell (SMC). The fibroblast subtype CTHRC1+ represented the most transcriptionally activated pro-fibrotic subtype, showing the greatest upregulation of ECM biosynthesis genes, a prominent role in intercellular communication, and preferential enrichment within fibroblastic foci in IPF lung tissue. Pseudotime trajectory analysis supported a directional transcriptional continuum from alveolar and inflammatory fibroblasts toward the CTHRC1+ state, driven by coordinated activation of pro-fibrotic transcription factors, including RUNX2, CREB3L1, and SCX. In vitro culture progressively reshaped fibroblast transcriptional identity relative to native tissue, with increased collagen and matrix metalloproteinase (MMP) expression during passaging, loss of distinct CTHRC1+ fibroblasts, and gain of alveolar fibroblasts displaying pro-fibrotic activation across all isolation protocols. These findings provide a high-resolution transcriptional map of lung fibroblast heterogeneity in IPF and highlight critical limitations of standard in vitro culture systems for recapitulating native fibroblast diversity, with important implications for the development and evaluation of fibroblast-targeted therapeutic strategies in IPF.

  PublisherOA PDFDOI

• RNAseq (with probes) data from the lung (right) of a 24 year-old white male

  Cellular Senescence Network (SenNet) · 2026-02-17

  datasetOpen access
  PublisherDOI

Recent grants

• Signaling mechanisms by which mitochondria regulates fibrosis in the lung

  NIH · $435k · 2016–2020

• NIH Grant R13HL124870

  NIH · $26k · 2015

• NIH Grant K01HL073154

  NIH · $641k · 2008

• Mapping Age-Related Changes in the Lung

  NIH · $2.4M · 2019–2025

• Biospecimen-Core

  NIH · $16.2M · 2021–2026

Frequent coauthors

• Mauricio Rojas

  The Ohio State University

  131 shared

• Marta Bueno

  University of Pittsburgh

  53 shared

• Lorena Rosas

  The Ohio State University

  45 shared

• Mark Boothby

  Vanderbilt University Medical Center

  41 shared

• Elena A. Goncharova

  University of California, Davis

  31 shared

• Mauricio Rojas

  Lung Institute

  29 shared

• John Sembrat

  The Ohio State University

  29 shared

• Mark T. Gladwin

  University of Maryland, Baltimore

  28 shared

Awards & honors

• Sidney P. Colowick Award for Outstanding Post-Doctoral Fello…
• AAI Minority Scientist American Association of Immunologists…
• Research Award, Münchner Bank HelmholtzZentrum Munich, 3rd M…
• Research Award, Pulmonary Fibrosis Foundation Summit (2013)