Journal
CELL METABOLISM
Volume 33, Issue 9, Pages 1853-+Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2021.08.002
Keywords
-
Categories
Funding
- US National Institutes of Health (NIH) [R01-DK55758, R01-DK127274, R01-DK099110, RC2 DK118620, P01-AG051459, K99DK122019]
- Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) [414232833]
- NIH [K01-DK125447]
- DFG Heisenberg professorship [Fi1700/7-1]
Ask authors/readers for more resources
Adipocytes under energetic stress release sEVs containing damaged mitochondrial particles, which enter circulation and trigger antioxidant signaling in cardiomyocytes, protecting them from oxidative stress. This functional mitochondrial transfer between tissues provides potent cardio-protection against stresses induced by obesity.
Adipocytes undergo intense energetic stress in obesity resulting in loss of mitochondrial mass and function. We have found that adipocytes respond to mitochondrial stress by rapidly and robustly releasing small extra cellular vesicles (sEVs). These sEVs contain respiration-competent, but oxidatively damaged mitochondrial particles, which enter circulation and are taken up by cardiomyocytes, where they trigger a burst of ROS. The result is compensatory antioxidant signaling in the heart that protects cardiomyocytes from acute oxidative stress, consistent with a preconditioning paradigm. As such, a single injection of sEVs from energetically stressed adipocytes limits cardiac ischemia/reperfusion injury in mice. This study provides the first description of functional mitochondrial transfer between tissues and the first vertebrate example of inter-organ mitohormesis.Thus, these seemingly toxic adipocyte sEVs may provide a physiological avenue of potent cardio-protection against the inevitable lipotoxic or ischemic stresses elicited by obesity.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available