Proteins are the fundamental drivers of biological function, orchestrating processes that range from metabolism and signal transduction to growth, immune defense, and tissue repair. Dysregulation of protein function lies at the heart of many human diseases, including lung injury and cancer. My research is centered on elucidating the molecular mechanisms by which proteins and subcellular systems govern disease initiation and progression. By integrating advanced protein analysis with the study of subcellular dynamics, we can define pathogenic signaling pathways, identify disease-specific vulnerabilities, and inform the development of precise diagnostic and therapeutic strategies.

The Power of Protein Analysis in Understanding Disease

Protein analysis is indispensable for mechanistic investigation in molecular medicine. Techniques such as Western blotting, immunoprecipitation, mass spectrometry–based proteomics, and subcellular fractionation enable both quantitative and qualitative assessment of protein abundance, post-translational modifications, interaction networks, and compartment-specific signaling.

In my work, these approaches are applied to investigate how oxidative stress disrupts lung cellular homeostasis. Perturbations in redox balance induce oxidative protein modifications, destabilize mitochondrial and inflammatory regulators, and activate maladaptive stress-response pathways. These molecular events contribute to the pathogenesis of bronchopulmonary dysplasia (BPD), acute lung injury, and lung cancer. By monitoring alterations in proteins involved in tissue repair, apoptosis, metabolism, and immune activation, we reconstruct the molecular cascade linking cellular stress to progressive tissue pathology.

Protein-level analyses further enable identification of critical nodes at which signaling fidelity collapses—such as aberrant phosphorylation of stress kinases, degradation of repair-associated proteins, or impaired antioxidant responses. These mechanistic insights form the foundation for rational therapeutic target selection.

Subcellular Dynamics: Understanding How Disease Emerges Within the Cell

While protein analysis addresses what changes occur in disease, the study of subcellular dynamics helps us understand how and where these changes take place. Cells contain specialized organelles—mitochondria, lysosomes, peroxisomes, and the endoplasmic reticulum—that function as coordinated systems. When communication between these organelles breaks down, disease processes often accelerate.

A significant focus of my research is mitochondrial dysfunction, which plays a central role in both lung injury and cancer. Damaged mitochondria generate excessive reactive oxygen species and fail to meet the energy demands of the cell. In neonatal lung injury, mitochondrial stress disrupts normal lung development, contributing to BPD. In cancer, mitochondrial reprogramming supports rapid cell proliferation, alters metabolic flux, and enhances resistance to cell death.

Cancer cells exploit subcellular dynamics to their advantage—altering organelle communication, hijacking quality control mechanisms, and reconfiguring metabolic networks. By mapping these alterations, we can identify vulnerabilities unique to tumor cells.

Connecting the Dots: From Molecular Mechanisms to Therapeutic Targets

The integration of protein biochemistry with subcellular analysis yields a systems-level understanding of disease mechanisms. By assessing both the molecular identity of dysregulated proteins and the subcellular context in which these changes occur, we can construct detailed mechanistic models of disease progression.

For example, protein translocation studies using cell fractionation reveal how stress-response proteins redistribute between cellular compartments during injury. Mass spectrometry–based interactomics identifies protein-protein interaction hubs that serve as regulatory control points. Mapping these interactions helps pinpoint nodes where targeted intervention may restore balanced signaling.

One active area of my research involves mitochondrial quality control pathways, particularly mitophagy. Impaired clearance of damaged mitochondria leads to the accumulation of dysfunctional organelles, persistent ROS production, and propagation of injury signals. In lung epithelial cells, restoring mitophagy has the potential to mitigate oxidative damage. In contrast, many cancer cells rely on selective manipulation of mitophagy to maintain metabolic fitness, making these pathways attractive targets for antitumor therapy.

Such integrated analyses bridge molecular mechanisms and therapeutic strategies, guiding the development of biomarker-driven interventions.

Looking Ahead: Advancing Molecular Medicine

Rapid technological advances continue to expand our ability to interrogate cellular systems with unprecedented resolution. Quantitative proteomics, phosphoproteomics, super-resolution imaging, CRISPR-based functional screens, and computational modeling now permit multidimensional analysis of protein behavior and organelle function. When combined with machine learning and systems biology, these tools enable integration of large-scale datasets and discovery of regulatory architectures previously inaccessible through conventional methods.

My future work aims to leverage these technologies to further define the molecular pathways driving lung injury and cancer, identify early-stage biomarkers, and develop mechanistically targeted therapeutic approaches with translational impact.

Conclusion

Protein analysis and subcellular dynamics together provide a powerful framework for understanding disease at the molecular level. These approaches illuminate how cells respond to injury, how organelle networks become disrupted, and which molecular events initiate or sustain pathology. Each mechanistic insight advances our capacity to design precise diagnostics and targeted therapies.

My overarching goal is to translate molecular discovery into interventions that improve human health. Guided by rigorous experimentation and translational intent, this work seeks to connect fundamental biology with meaningful clinical outcomes in lung injury and cancer..