In mice with obesity, a type of immune cell called neutrophils in the heart show increased activity of specific genes linked to inflammation, which may be related to heart stress caused by obesity.
Mechanism
Synthesis from 1 study
In obese mice, immune cells called neutrophils go into the heart and start releasing chemicals that attract more immune cells and cause damage. These chemicals create stress in heart tissue, which can harm its function over time.
Most probable mechanism
In obese mice, a type of immune cell called neutrophils enter the heart and turn on genes that release inflammatory signals. These signals attract more immune cells and cause damage through chemical stress, leading to heart tissue stress.
Neutrophils accumulate in cardiac tissue under conditions of obesity.
Neutrophils in cardiac tissue upregulate expression of the genes Cxcl2, S100a8, and S100a9.
Cxcl2 protein secreted by neutrophils acts as a chemokine to recruit additional immune cells into cardiac tissue.
S100a8 and S100a9 proteins form a complex that activates Toll-like receptor 4 signaling, triggering production of reactive oxygen species and pro-inflammatory cytokines.
Increased oxidative stress and cytokine release in cardiac tissue leads to cellular damage and functional stress.
Evidence from Studies
Supporting (1)
Community contributions welcome
Contradicting (0)
Community contributions welcome
Gold Standard Evidence Needed
According to GRADE and EBM methodology, here is what ideal scientific evidence would look like to definitively prove or disprove this specific claim, ordered from strongest to weakest evidence.