Difference between revisions of "Liu 2018 Atherosclerosis Suppl"
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|event=Atherosclerosis Suppl | |event=Atherosclerosis Suppl | ||
|abstract=Inhibition of transient receptor potential channel, canonical type 3 (TRPC3) attenuates monocytes and vasculature calcium influx in spontaneously hypertensive rats (SHRs). However, it remains elusive whether mitochondrial TRPC3 participates in increasing mitochondrial calcium homeostasis and ROS production in monocytes from hypertension. | |abstract=Inhibition of transient receptor potential channel, canonical type 3 (''TRPC3'') attenuates monocytes and vasculature calcium influx in spontaneously hypertensive rats (SHRs). However, it remains elusive whether mitochondrial ''TRPC3'' participates in increasing mitochondrial calcium homeostasis and ROS production in monocytes from hypertension. | ||
|editor=[[Plangger M]], [[Kandolf G]], | |editor=[[Plangger M]], [[Kandolf G]], | ||
|mipnetlab=CN Chongqing Zhu Z | |mipnetlab=CN Chongqing Zhu Z |
Revision as of 15:06, 22 August 2018
Liu D (2018) Enhanced Trpc3-mediated mitochondrial respiratory dysfunction by inhibition of mitochondria-hexokinase in monocytes from hypertension rats. Atherosclerosis Suppl. |
Link: Atherosclerosis
Liu D (2018)
Event: Atherosclerosis Suppl
Inhibition of transient receptor potential channel, canonical type 3 (TRPC3) attenuates monocytes and vasculature calcium influx in spontaneously hypertensive rats (SHRs). However, it remains elusive whether mitochondrial TRPC3 participates in increasing mitochondrial calcium homeostasis and ROS production in monocytes from hypertension.
β’ Bioblast editor: Plangger M, Kandolf G
β’ O2k-Network Lab: CN Chongqing Zhu Z
Labels: MiParea: Respiration, nDNA;cell genetics
Organism: Rat
Tissue;cell: Blood cells
Preparation: Intact cells
Coupling state: ROUTINE, OXPHOS, ET
Pathway: N, NS
HRR: Oxygraph-2k
Affiliations
- Daping Hospital, Third Military Medical Univ, Chongqing, China