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. Author manuscript; available in PMC: 2015 Apr 6.
Published in final edited form as: Can J Physiol Pharmacol. 2014 Nov 25;93(2):97–110. doi: 10.1139/cjpp-2014-0361

Fig. 10.

Fig. 10

Inflammatory cytokines induce ROS generation in hASM that leads to ER/SR stress with downstream impact of reduced Mfn2 expression (increased Drp1), uncoupling of mitochondria to the ER/SR membrane, decreased [Ca2+]mito buffering, which contributes to increased [Ca2+]cyt and force responses to ACh stimulation (hyper-reactive state). A decrease in [Ca2+]mito buffering also leads to mitochondrial dysfunction and a further increase in ROS generation. Reduced Mfn2 expression also leads to mitochondrial fragmentation (fission) and increased cell proliferation and remodeling (synthetic state). ROS, reactive oxidant species; hASM, human airway smooth muscle cells; ER/SR, endoplasmic reticulum/sarcoplasmic reticulum; ACh, acetycholine; Mfn2, mitofusin-2; Drp1, dynamin related protein 1.