Profile image for Anis S. Hanna

Anis S. Hanna, M.B.,B.Ch.

Area of research

  • Heart Failure, Myocardial Infarction, Fibrosis, Cardiac Inflammation, Diabetic Cardiomyopathy, TGF-beta, Omics, scRNAseq

Email

Location

  • Albert Einstein College of Medicine Jack and Pearl Resnick Campus 1300 Morris Park Avenue Forchheimer Building G45 Bronx, NY 10461

Research Profiles

Research Profiles

Professional Interests

I have a profound passion for dissecting the molecular and cellular mechanisms of cardiac fibrosis and remodeling, and my goal is to identify novel therapeutic targets for heart failure patients.

My current focus is on solving a central dilemma in cardiovascular medicine: how to stop the pathological, expansive fibrosis that drives heart failure without compromising the essential, reparative scar that prevents cardiac rupture after a myocardial infarction (MI). To address this, we move beyond studying fibrosis as a monolithic process. Instead, our mission is to unravel the cellular heterogeneity that orchestrates cardiac repair, hypothesizing that the key to new therapies lies in understanding how different cell populations are organized in space and time. The ultimate goal is to target pathological infarct cell subpopulations while preserving the beneficial role of other subsets.

To achieve this, we employ multi-modal omics to build and analyze atlas-level, spatiotemporal datasets of the healing heart. We use single-cell and spatial multi-omics to simultaneously map the transcriptome and epigenome of every cell in its native tissue context. We complement this with sequential immunofluorescence for high-plex spatial proteomics. Our integrative bioinformatics and machine learning-based image analysis enable us to integrate these multi-layered big data into a cohesive understanding of cardiac injury and repair.

This work builds upon our foundational expertise and published studies exploring the role of TGF-beta/Smad signaling in cardiac remodeling (Circ Res 2019, JCI 2022), the mechanisms of cardiac rupture (AJP-Heart 2020), and collagen degradation in the infarct scar (Matrix Biology 2021). Our recent high-impact work deciphering the heterogeneity of cardiac pericytes in diabetes (JAHA 2023) and MI (Circulation 2023) uncovered novel pericyte complexity in heart disease. In addition to our ambitious work uncovering the protective role of Smad1 in a regulatory myofibroblast subpopulation following MI (manuscript under revision & selected for the American Heart Association's Katz Award for Early Stage Investigators).

Selected Publications

  1. Li R, Huang S, Hanna A, et al. Macrophage ITGAV is dispensable for post-infarction remodeling in mice and does not mediate fibronectin responses. Commun Biol (2025). https://doi.org/10.1038/s42003-025-09295-y
  2. Qin D, Modanwal R, Ghazi M, Corbalan J, Jia F, Axelrod J, Mesidor R, Jang H, Humeres C, Hanna A, et al. Reformulation of the Necroptosis Pathway in Reperfused Myocardial Infarction. Circulation. 2025;152(7):486-488. doi:10.1161/CIRCULATIONAHA.124.073023
  3. Li R#, Hanna A#, Huang S, Hernandez SC, Tuleta I, Kubota A, et al. Macrophages in the infarcted heart acquire a fibrogenic phenotype, expressing matricellular proteins, but do not undergo fibroblast conversion. J Mol Cell Cardiol. 2024;196:152–67. Epub 20240731. doi: 10.1016/j.yjmcc.2024.07.010. PubMed PMID: 39089570; PubMed Central PMCID: PMC11534516.
    # co-first authors
  4. Humeres C, Shinde AV, Tuleta I, Hernandez SC, Hanna A, Huang S, et al. Fibroblast Smad7 Induction Protects the Remodeling Pressure-Overloaded Heart. Circ Res. 2024;135(3):453–69. Epub 20240620. doi: 10.1161/circresaha.123.323360. PubMed PMID: 38899461; PubMed Central PMCID: PMC11257802.
  5. Tuleta I, Hanna A, Humeres C, Aguilan JT, Sidoli S, Zhu F, et al. Fibroblast-specific TGF-beta signaling mediates cardiac dysfunction, fibrosis, and hypertrophy in obese diabetic mice. Cardiovasc Res. 2024;120(16):2047–63. doi: 10.1093/cvr/cvae210. PubMed PMID: 39373248; PubMed Central PMCID: PMC12097992.
  6. Alex L, Tuleta I, Hernandez SC, Hanna A, Venugopal H, Astorkia M, et al. Cardiac Pericytes Acquire a Fibrogenic Phenotype and Contribute to Vascular Maturation After Myocardial Infarction. Circulation. 2023;148(11):882–98. Epub 20230623. doi: 10.1161/circulationaha.123.064155. PubMed PMID: 37350296; PubMed Central PMCID: PMC10527624.
  7. Li R, Chen B, Kubota A, Hanna A, Humeres C, Hernandez SC, et al. Protective effects of macrophage-specific integrin alpha5 in myocardial infarction are associated with accentuated angiogenesis. Nat Commun. 2023;14(1):7555. Epub 20231120. doi: 10.1038/s41467-023-43369-x. PubMed PMID: 37985764; PubMed Central PMCID: PMC10662477.
  8. Qin D, Jia XF, Hanna A, Lee J, Pekson R, Elrod JW, et al. BAK contributes critically to necrosis and infarct generation during reperfused myocardial infarction. J Mol Cell Cardiol. 2023;184:1–12. Epub 20230912. doi: 10.1016/j.yjmcc.2023.09.004. PubMed PMID: 37709008; PubMed Central PMCID: PMC10841630.
  9. Alex L, Tuleta I, Hanna A, Frangogiannis NG. Diabetes Induces Cardiac Fibroblast Activation, Promoting a Matrix- Preserving Nonmyofibroblast Phenotype, Without Stimulating Pericyte to Fibroblast Conversion. J Am Heart Assoc. 2023;12(6):e027463. Epub 20230309. doi: 10.1161/jaha.122.027463. PubMed PMID: 36892073; PubMed Central PMCID: PMC10111546.
  10. Li J, Li R, Tuleta I, Hernandez SC, Humeres C, Hanna A, et al. The role of endogenous Smad7 in regulating macrophage phenotype following myocardial infarction. Faseb j. 2022;36(7):e22400. doi: 10.1096/fj.202101956RR. PubMed PMID: 35695814; PubMed Central PMCID: PMC9216182.
  11. Venugopal H, Hanna A, Humeres C, Frangogiannis NG. Properties and Functions of Fibroblasts and Myofibroblasts in Myocardial Infarction. Cells. 2022;11(9). Epub 20220420. doi: 10.3390/cells11091386. PubMed PMID: 35563692; PubMed Central PMCID: PMC9102016.
  12. Chen B, Li R, Hernandez SC, Hanna A, Su K, Shinde AV, et al. Differential effects of Smad2 and Smad3 in regulation of macrophage phenotype and function in the infarcted myocardium. J Mol Cell Cardiol. 2022;171:1–15. Epub 20220701. doi: 10.1016/j.yjmcc.2022.06.009. PubMed PMID: 35780861.
  13. Humeres C, Shinde AV, Hanna A, Alex L, Hernandez SC, Li R, et al. Smad7 effects on TGF-beta and ErbB2 restrain myofibroblast activation and protect from postinfarction heart failure. J Clin Invest. 2022;132(3). doi: 10.1172/jci146926. PubMed PMID: 34905511; PubMed Central PMCID: PMC8803336.
  14. Hanna A, Humeres C, Frangogiannis NG. The role of Smad signaling cascades in cardiac fibrosis. Cell Signal. 2021;77:109826. Epub 20201105. doi: 10.1016/j.cellsig.2020.109826. PubMed PMID: 33160018; PubMed Central PMCID: PMC7727442.
  15. Hanna A, Shinde AV, Li R, Alex L, Humeres C, Balasubramanian P, et al. Collagen denaturation in the infarcted myocardium involves temporally distinct effects of MT1-MMP-dependent proteolysis and mechanical tension. Matrix Biol. 2021;99:18–42. Epub 20210525. doi: 10.1016/j.matbio.2021.05.005. PubMed PMID: 34048934; PubMed Central PMCID: PMC8591556.
  16. Hanna A, Shinde AV, Frangogiannis NG. Validation of diagnostic criteria and histopathological characterization of cardiac rupture in the mouse model of nonreperfused myocardial infarction. Am J Physiol Heart Circ Physiol. 2020;319(5):H948–h64. Epub 20200904. doi: 10.1152/ajpheart.00318.2020. PubMed PMID: 32886000; PubMed Central PMCID: PMC7701358.
  17. Huang S, Chen B, Humeres C, Alex L, Hanna A, Frangogiannis NG. The role of Smad2 and Smad3 in regulating homeostatic functions of fibroblasts in vitro and in adult mice. Biochim Biophys Acta Mol Cell Res. 2020;1867(7):118703. Epub 20200314. doi: 10.1016/j.bbamcr.2020.118703. PubMed PMID: 32179057; PubMed Central PMCID: PMC7261645.
  18. Hanna A, Frangogiannis NG. Inflammatory Cytokines and Chemokines as Therapeutic Targets in Heart Failure. Cardiovasc Drugs Ther. 2020;34(6):849–63. Epub 20200909. doi: 10.1007/s10557-020-07071-0. PubMed PMID: 32902739; PubMed Central PMCID: PMC7479403.
  19. Hanna A, Frangogiannis NG. The cell biological basis for primary unloading in acute myocardial infarction. Int J Cardiol. 2019;293:45–7. Epub 20190702. doi: 10.1016/j.ijcard.2019.06.079. PubMed PMID: 31296394.
  20. Chen B, Huang S, Su Y, Wu YJ, Hanna A, Brickshawana A, et al. Macrophage Smad3 Protects the Infarcted Heart, Stimulating Phagocytosis and Regulating Inflammation. Circ Res. 2019;125(1):55–70. Epub 20190516. doi: 10.1161/circresaha.119.315069. PubMed PMID: 31092129; PubMed Central PMCID: PMC6681442.
  21. Russo I, Cavalera M, Huang S, Su Y, Hanna A, Chen B, et al. Protective Effects of Activated Myofibroblasts in the Pressure-Overloaded Myocardium Are Mediated Through Smad-Dependent Activation of a Matrix- Preserving Program. Circ Res. 2019;124(8):1214–27. doi: 10.1161/circresaha.118.314438. PubMed PMID: 30686120; PubMed Central PMCID: PMC6459716.
  22. Hanna A, Frangogiannis NG. The Role of the TGF-beta Superfamily in Myocardial Infarction. Front Cardiovasc Med. 2019;6:140. Epub 20190918. doi: 10.3389/fcvm.2019.00140. PubMed PMID: 31620450; PubMed Central PMCID: PMC6760019.