Making the invisible visible since 2013
Mitocare Center
MitoCare Center for Mitochrondrial Imaging Research & Diagnostics
Leveraging Technology to Innovate & Create in the Study of Mitochondria
At the Center (referred to as MitoCare Center), our team pairs advanced, high-resolution 3D imaging modalities in vitro and in vivo with other cutting-edge technologies to study mitochondrial health and disease pathogenesis, diagnostics, and potential therapeutic targets.
Our Mission is to innovate, create, and use advanced technologies in a programmatic context to study mitochondria in health and disease.
Why Mitochondria?
Historically, we thought mitochondria were just the powerhouses of the cell.
This has never been true.
Mitochondria are the most interactive organelles in the eukaryotic cell. With only 1.4% of the human genome controlling their function, mitochondria have the striking capability to govern a multitude of cellular functions, from metabolism and ion homeostasis to cell fate and immunity.
Latest from the Center
New Publication
OPA1 Modulates Mitochondrial Ca2+ Uptake Through ER-Mitochondria Coupling
Congratulations to Benjamín for his Frontiers in Cell and Developmental Biology publication with Dr. Eisner and Dr. Hajnóczky.
Dwell into how OPA1 regulates functional ER-mitochondria contact sites that mediate Ca2+ transfer to mitochondria.
New Funding
MRIE Team Science Grant was awarded to the team of Drs. Hajnoczky-Terai-Wedegartner to Develop Novel Therapeutics for Uveal Melanoma
The 2-year project also includes Piyush Mishra. The team will study the role of altered mitochondrial calcium signaling in uveal melanoma pathogenesis and a new therapeutic strategy to induce apoptosis selectively in the tumor metastases in the liver.
Breaking News
Welcome to Dr. Rajarshi Chakrabarti that joined the MitoCare team as Assistant Professor in August 2022
Dr. Chakrabarti recently uncovered how dysfunctional mitochondria recall the cytoskeleton to promote rapid actin polymerization. At MitoCare, he will continue his journey toward deciphering the different modalities and triggers conducive to mitochondrial stress signaling.
New Publication
Capture at the ER-mitochondrial contacts licenses IP3 receptors to stimulate local Ca2+ transfer and oxidative metabolism
ER-Mitochondria contacts are central to life but how they are formed and dissolved is unclear. Here, the Hajnoczky lab shows that the IP3 receptor traffics in and out of the contacts and, when trapped, improves calcium signaling to stimulate energy metabolism.