Ana Mora, MD

  • Director Education, Aging Institute
  • Director, Small Animal Hemodynamic Core
  • Associate Professor of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, Vascular Medicine Institute

Education & Training

  • Medical School - Universidad Nacional de Columbia Medical School - MD
  • Post-Doctoral Fellow – Universidad Nacional de Columbia - Molecular Immunology
  • Post-Doctoral Fellow – Vanderbilt University - Microbiology and Immunology

Research Grants

NIH Grants:  K01, P01, R01

Research Summary

The research in Dr. Mora’s lab is focused in the elucidation of the pathogenic mechanisms of Idiopathic Pulmonary Fibrosis (IPF). Because aging is a main risk factor of IPF, studies in Dr. Mora’s lab examine how aging-related cell perturbations contribute to the injury and fibrosis observed in the lungs of IPF patients. Dr. Mora’s group pioneered aging studies showing mitochondrial dysfunction in alveolar type II lung epithelial cells from lungs of IPF patients, the alterations in mitochondria were associated with deficiencies in mitochondrial homeostasis and insufficient mitophagy. Seminal studies from Dr. Mora’s lab have shown that deficiency in mitochondrial function in lung epithelial cells involves complex interactions with cellular stress pathways. In addition, her group has discovered that alterations in mitochondrial homeostasis drives senescence phenotype in lung cells and activate profibrotic responses by the release of mitochondrial damage associated molecular pattern (DAMPs). Currently, using single cell RNAseq data from human lung samples, Dr. Mora’s lab is characterizing transcriptomic age- and disease-related changes in mitochondrial nuclear-encoded genes. These studies have important implications in the definition of key elements in how mitochondria and metabolic reprogramming are involved in lung aging, the pathogenesis of IPF, and potential definition of novel biomarkers of disease severity. Finally, toward potential therapies, Dr. Mora’s group is analyzing mitochondrial-targeted therapies in animal models of lung fibrosis. Another focus of Dr. Mora’s lab is how mitochondrial dysfunction contributes to vascular remodeling and the development with age of cardiovascular diseases and hypertension. Dr. Mora’s laboratory utilizes biochemical and molecular studies, in vitro analysis of human bio-specimens, animal models of lung fibrosis and pulmonary hypertension. Her lab has developed numerous novel genetically modified murine models to define in vivo the role of mitochondrial targets. She is actively involved in research training of undergraduate students, post-doctoral fellows and pulmonary fellows.

Representative Publications

  1. Bueno M, Lai YC, Romero Y, Brands J, St Croix CM, Kamga C, Corey C, Herazo-Maya JD, Sembrat J, Lee JS, Duncan SR, Rojas M, Shiva S, Chu CT, Mora AL.  PINK1 deficiency impairs mitochondrial homeostasis and promotes lung fibrosis. J Clin Invest. 2015 Feb;125(2):521-38. doi: 10.1172/JCI74942. Epub 2014 Dec 22. PubMed PMID: 25562319; PubMed Central PMCID: PMC4319413.
  2. Mora AL, Bueno M, Rojas M. Mitochondria in the spotlight of aging and idiopathic pulmonary fibrosis. J Clin Invest. 2017 Feb 1;127(2):405-414. doi: 10.1172/JCI87440. Epub 2017 Feb 1. Review. PubMed PMID: 28145905; PubMed Central. PMCID: PMC5272191.
  3. Bueno M, Brands J, Voltz L, Fiedler K, Sembrat J, Mallampalli RK, Rojas M, and Mora AL. ATF3 represses PINK1 gene transcription in lung epithelial to control mitochondrial homeostasis. 2018, Aging Cell, 17(2).PMID 2936323258.
  4. Mora AL, Rojas M, Pardo A, Selman M. Emerging therapies for idiopathic pulmonary fibrosis, a progressive age-related disease. Nat Rev Drug Discov. 2017 Nov;16(11):755-772. doi: 10.1038/nrd.2017.170. Epub 2017 Oct 6. Review. Erratum in: Nat Rev Drug Discov. 2017 Oct 30;16(11):810. PubMed PMID: 28983101.
  5. Lai YC, Tabima DM, Dube JJ, Hughan KS, Vanderpool RR, Goncharov DA, St Croix CM, Garcia-Ocaña A, Goncharova EA, Tofovic SP, Mora AL, Gladwin MT. SIRT3-AMP-Activated Protein Kinase Activation by Nitrite and Metformin Improves Hyperglycemia and Normalizes Pulmonary Hypertension Associated With Heart Failure With Preserved Ejection Fraction. Circulation. 2016 Feb 23;133(8):717-31. doi: 10.1161/CIRCULATIONAHA.115.018935. Epub 2016 Jan 26. PubMed PMID: 26813102; PubMed Central PMCID: PMC4766041.
  6. Romero Y, Bueno M, Ramirez R, Alvarez D, Sembrat J, Goncharova EA, Rojas M, Selman M, Mora AL, Pardo A. mTORC1 activation decreases autophagy in aging and idiopathic pulmonary fibrosis and contributes to apoptosis resistance in IPF fibroblasts. Aging Cell, 2016, PMID 27566137.Co-senior author