About

Ravi Radhakrishnan, Ph.D., holds the title of Professor of Bioengineering and Professor of Chemical and Biomolecular Engineering at the University of Pennsylvania. He is a member of the Genomics & Computational Biology and the Biochemistry & Molecular Biophysics graduate groups. He is a founder member and served as the former Director of the Penn Institute for Computational Sciences, an interdisciplinary institute promoting research at the interface of multiscale modeling, machine learning, and high-performance supercomputing. His research interests are at the interface of biophysics, biomolecular engineering, and bioengineering, with a focus on creating Digital Twin Models in Biomedical Engineering for Cancer Treatment and Next Generation Therapeutics using Nanomedicine. His laboratory specializes in computational algorithms spanning molecular and cellular scales, utilizing statistical mechanics, machine learning, artificial intelligence, and high-performance scientific computing in parallel architectures.

Research topics

• Biology
• Biochemistry
• Cell biology
• Computer Science
• Cancer research
• Artificial Intelligence
• Engineering
• Physics
• Genetics
• Biochemical engineering
• Chemistry
• Data science

Selected publications

• MYC and AP-1 oncogenes cooperatively bind enhancers to rewire transcription

  NAR Cancer · 2026-03-26

  articleOpen access

  motif discovery analysis on published MYC ChIP-seq datasets from cancer cell lines, we found cell-type-specific co-enrichment of the TRE motifs (AP-1 binding sites) alongside MYC's canonical EBOX motif. MYC binds indirectly to TRE motifs in cooperation with AP-1 transcription factors, and these indirect interactions occur predominantly at enhancers rather than promoters. At elevated MYC levels, as seen in cancers, MYC's indirect binding to TRE sites at enhancers increases. Integration of ChIP-seq and RNA sequencing data revealed that TRE enhancer-binding sites are frequently associated with MYC-mediated transcriptional repression. Gene Ontology analysis showed that MYC utilizes TRE sites to transcriptionally rewire cells, modulating cancer hallmarks like proliferation, apoptosis, and cell adhesion. These molecular insights into how increased MYC levels alter gene regulation could inform new therapeutic strategies targeting cancer-specific MYC functions and its co-regulators.

  PublisherDOI

• Circulating Factors Induce Cardiomyopathy after Burn Injury

  Journal of the American College of Surgeons · 2026-03-26

  articleSenior authorCorresponding

  BACKGROUND: Previous in vivo work has demonstrated that the phosphodiesterase type 5 (PDE5)-cyclic guanosine monophosphate-protein kinase G pathway is involved in burn-induced heart dysfunction. PDE5A inhibitors may reverse this dysfunction. It is unknown if circulating factors after burn injury can continue to damage cardiomyocytes and if this can be reversed by PDE5A inhibitors in vitro. This study hypothesized that circulating factors released after burn injury cause mitochondrial damage in cardiomyocytes in vitro. STUDY DESIGN: Human cardiomyocyte cell line-AC16-was divided into 4 groups, which were treated with serum obtained from rats with sham injury, 24 hours post burn (24hpb), sildenafil (SIL) alone, and 24hpb treated with SIL. ELISA, mitochondrial function studies, fluorescence microscopy, gene analysis, and Illumina RNA sequencing were performed. GraphPad Prism 9.2.0 was used for statistical analysis. RESULTS: Cyclic guanosine monophosphate levels were significantly decreased, and cTN1 levels were significantly increased in the 24hpb serum group. Treatment with SIL completely reversed this change, similar to our previous in vivo work. We observed that there was significantly decreased cell viability and cell proliferation and increased cell cytotoxicity, cell apoptosis, and cell reactive oxygen species production in the cells treated with 24hpb serum. Cells treated with 24hpb serum exhibited mitochondrial dysfunction, as demonstrated by decreased ATP production and compromised mitochondrial membrane integrity or potential, along with increased mitochondrial reactive oxygen species. Seahorse and O2K approaches confirmed 24hpb serum treated cardiomyocyte mitochondrial dysfunction as evidenced by decreases in mitochondrial basal respiration, proton leak, ATP production, and maximal respiration. SIL returned these responses to near sham levels. CONCLUSIONS: This study provided data that may improve the understanding of mechanisms driving cardiac dysfunction after burn injury. Our study provided evidence for understanding the pathogenic mechanism of circulating factors released after burn injury.

  PublisherDOI

• Further Considerations in Pediatric Appendicitis—Reply

  JAMA Pediatrics · 2026-02-02

  articleSenior author
  PublisherDOI

• BPS2026 – Tissue-dependent mechanosensing by cells derived from human tumors

  Biophysical Journal · 2026-02-01

  articleSenior author
  PublisherDOI

• Data from: Modeling tumor transport and growth with poroelastic biopolymer networks

  Open MIND · 2026-03-28

  datasetOpen access

  The mechanical properties of the extracellular matrix (ECM) regulate tumor growth and invasion in the tumor microenvironment. Models of biopolymer networks have been used to investigate the impact of the elasticity and viscoelasticity of ECM on tumor behavior. Under tumor compression, these networks also show poroelastic behavior that is governed by the resistance to water flow through their pores. This work investigates the hypothesis that stress-dependent transport properties of biopolymer networks regulate tumor growth. Here, alginate hydrogels are used as a model ECM system with tunable ionic and hybrid ionic/covalent crosslinking. Hydrogel stiffness, viscoelasticity, and stress relaxation behavior were characterized using stepwise axial compression. Among these properties, we find that poroelastic fluid outflow dominates ECM stress relaxation, as the measured water flux was significantly affected under compression. Continuum mechanics-based modeling was developed to formulate and calculate the chemical potential gradients of water (solvent) in the hydrogels under compression. This framework was extended into an advection-diffusion framework to quantify growth factor (solute) distribution under varying strengths of stress and diffusion indexed by the relative strength of convective to diffusive transport, characterized by the Péclet number. An agent-based computational simulation showed that the Péclet numbers based on our experimental timescales strongly influenced tumor growth over longer, more physiologic timescales. Together, these results highlight the important role of water flux and transport in three-dimensional biopolymer networks.

  PublisherDOI

• MYC and AP-1 oncogenes cooperatively bind enhancers to rewire transcription

  Open MIND · 2026-03-10

  other

  Kalyan Sundaram et al, "MYC and AP-1 oncogenes cooperatively bind enhancers to rewire transcription", NAR Cancer 2026 This folder contains codes, figure generation scripts and sample analyses runs used in this study.

  DOI

• MYC and AP-1 oncogenes cooperatively bind enhancers to rewire transcription

  Zenodo (CERN European Organization for Nuclear Research) · 2026-03-10

  otherOpen access

  Kalyan Sundaram et al, "MYC and AP-1 oncogenes cooperatively bind enhancers to rewire transcription", NAR Cancer 2026 This folder contains codes, figure generation scripts and sample analyses runs used in this study.

  PublisherDOI

• RPPA data and analysis for melanoma cells under tryptophan deprivation

  Open MIND · 2026-01-29

  other
  DOI

• RPPA data and analysis for melanoma cells under tryptophan deprivation

  Zenodo (CERN European Organization for Nuclear Research) · 2026-01-29

  otherOpen access
  PublisherDOI

• Author Correction: Branched endosomal disruptor (BEND) lipids mediate delivery of mRNA and CRISPR-Cas9 ribonucleoprotein complex for hepatic gene editing and T cell engineering

  Nature Communications · 2025-10-07 · 2 citations

  erratumOpen access
  PublisherOA PDFDOI

Recent grants

• A plasticity and reprogramming paradigm for therapy resistance at the single cell level

  NIH · $3.3M · 2018–2023

• Biomolecular Simulations as an Integral Research and Educational Tool for Molecular Systems Biology: Application to ErbB

  NSF · $313k · 2009–2013

• Theory and Simulation of Membrane Deformations Orchestrated by Intracellular Molecular Assemblies

  NSF · $300k · 2009–2013

• Multiscale Modeling to Optimize Inhibition of Oncogenic ERK Pathway Signaling

  NIH · $3.4M · 2020–2025

• Surgical Research Training in Gastrointestinal Diseases

  NIH · $197k · 1992–2024

Frequent coauthors

• David M. Eckmann

  The Ohio State University

  67 shared

• P. S. Ayyaswamy

  University of California, Los Angeles

  60 shared

• Ramakrishnan Natesan

  University of Pennsylvania

  41 shared

• Vladimir R. Muzykantov

  Translational Therapeutics (United States)

  34 shared

• Tamar Schlick

  New York University

  33 shared

• Ryan Bradley

  Lehigh University

  33 shared

• Samaneh Farokhirad

  24 shared

• Małgorzata Śliwińska-Bartkowiak

  24 shared

Education

• Ph.D., Chemical Engineering

  University of Pennsylvania

  2000

• M.S., Chemical Engineering

  University of California, Berkeley

  1995

• B.S., Chemical Engineering

  University of Madras

  1993

Awards & honors

• Hewlett Packard Investigator Award
• Fellow of the American Institute of Medical and Biological E…
• Fellow of the Royal Society of Medicine
• Fellow of the Biomedical Engineering Society