Chandel Lab

Dr. Chandel discusses a recent study that may improve the understanding of mitochondrial dysfunction and its impact on the development of neurological diseases. The study, led by Greg McElroy, also suggests that targeting mitochondrial complex I linked biology could be a promising therapeutic target for neurological diseases.

Mitochondria, the organelle that powers most cells in the body, may be the canary in the coal mine for neurological disease, according to new findings published in the Journal of Cell Biology. Mitochondrial stress and dysfunction have long been suspected as an early step in diseases like Parkinson’s or Alzheimer’s disease, but Navdeep Chandel and collaborators have uncovered a mechanism that may explain how. The study found that mitochondrial stress in neurons can cause an enzyme imbalance that contributes to neuronal dysfunction and death. Reversing this imbalance showed promise in cell models, sketching an outline of a future therapy.

Northwestern Medicine scientists have demonstrated that a specific mitochondrial protein complex is essential to the immunosuppressive activity of regulatory T-cells, findings with potential significance for a wide variety of autoimmune diseases.

​

The study, published in Nature, demonstrated that the suppressive function of regulatory T (Treg) cells was impaired when they had been modified to lack mitochondria complex III, previously known as an essential component of mitochondrial function.

New Northwestern Medicine published in Nature Cell Biology has shown that mitochondria, traditionally known for their role creating energy in cells, also play an important role in hematopoiesis, the body's process for creating new blood cells.

​

In this study, Navdeep S. Chandel's lab, including postdoctoral fellow Elena Anso, PhD, and graduate students Sam Weinberg and Lauren Diebold demonstrated that mitochondria control hematopoietic stem cell fat by preventing the generation of a metabolite called 2-hydroxyglutarate (2HG). The scientists showed that mice with stem cells deficient in mitochondrial function cannot generate blood cells due to elevated levels of 2HG, which causes histone and DNA hyper-methylation.

Dr. Chandel discusses recent publications in the lab demonstrating the essential role of the mitochondrial electron transport chain in tumorigenesis and potential therapeutic avenues for targeting mitochondrial metabolism in the clinic.

Metabolic therapy is showing promise in robbing malignant cells of their primary energy source. In this Op-Ed, Navdeep Chandel discusses the current status and future directions of metabolic therapy in the clinic.

Clarivate Analytics has included Navdeep S. Chandel, PhD in their list of Highly Cited Researchers from 2018-2020. This list represents scientists and social scientists who have demonstrated significant influence in the last decade. It recognizes world-class researchers selected for their exceptional research performance, demonstrated by production of multiple highly cited papers that rank in the top 1% by citations for field and year in Web of Science.

Link to Google Scholar

In this article, Dr. Navdeep Chandel discusses the potential of Metformin as a drug to combat the COVID-19 pandemic.

Mitochondria are most famous as sources of metabolic energy. But by splitting and combining, they can also release chemical signals to regulate cell activities, including the generation of neurons.

Navdeep S. Chandel's lab has used an innovative gene editing technique to identify the genes that may lead to Parkinson's disease after exposure to paraquat, a commonly used herbicide. This study, which utilized the CRISPR-Cas9 gene-editing tool, serves as a proof-of-concept for using genetic screens to investigate the biology of oxidative stress.

​

The study was published in Nature Chemical Biology and the first author was Colleen Reczek, PhD, a postdoctoral fellow in Chandel's lab. Other authors include Chandel lab members Hyewon Kong and Inmaculada Martinez-Reyes, PhD.