Mitochondrial dysfunction in macrophages promotes inflammation and suppresses repair after myocardial infarction
University of Washington · Infectious Disease Research Institute
Abstract
Innate immune cells play important roles in tissue injury and repair following acute myocardial infarction (MI). Although reprogramming of macrophage metabolism has been observed during inflammation and resolution phases, the mechanistic link to macrophage phenotype is not fully understood. In this study, we found that myeloid-specific deletion (mKO) of mitochondrial complex I protein, encoded by Ndufs4, reproduced the proinflammatory metabolic profile in macrophages and exaggerated the response to LPS. Moreover, mKO mice showed increased mortality, poor scar formation, and worsened cardiac function 30 days after MI. We observed a greater inflammatory response in mKO mice on day 1 followed by increased cell…
Citation impact
- FWCI
- 36.64
- Percentile
- 100%
- References
- 45
Authors
10Topics & keywords
- Efferocytosis
- Inflammation
- Myofibroblast
- Proinflammatory cytokine
- Macrophage
- Cell biology
- Cancer research
- Mitochondrion
- Good health and well-being