Mallar Bhattacharya, MD is an Associate Professor of Medicine at the University of California, San Francisco. He earned both his bachelor’s and medical degrees from Harvard University, completed his residency in internal medicine at Johns Hopkins Hospital, and pursued fellowship training in pulmonary and critical care medicine at UCSF, where he now leads a research program focused on mechanisms of lung fibrosis.

Dr. Bhattacharya’s laboratory has made fundamental contributions to the understanding of immune-mesenchymal interactions in lung fibrosis. His work identified a transitional profibrotic lung macrophage population using single-cell RNA sequencing and developed SingleR, a widely adopted computational tool for annotating cell types in single-cell datasets. Dr. Bhattacharya went on to define novel paracrine circuits between myeloid cells and fibroblasts. In recent work, his laboratory has found that these interactions lead to the induction of myeloid Arg1 and elevated lung ornithine levels, a key substrate for collagen synthesis by fibroblasts. These findings were supported by parallel studies in mouse models and precision-cut lung slices from patients with idiopathic pulmonary fibrosis (IPF). Dr. Bhattacharya’s lab also conducted the first large-scale transcriptomic and functional study of human lung aging, identifying cellular senescence, telomere shortening, loss of alveolar type 2 epithelial cells, and expansion of mesenchymal populations as defining features.

Dr. Bhattacharya serves on national committees of the American Thoracic Society and the American Physiological Society, and on the editorial board of Comprehensive Physiology. A dedicated educator, Dr. Bhattacharya also directs the UCSF Inquiry Funding Office, supporting student research, and provides bedside teaching as a critical care attending at UCSF Medical Center. His work integrates clinical insight with rigorous laboratory investigation, computational innovation, and translational modeling to uncover mechanisms and therapeutic targets in fibrotic lung disease.