AI Article Synopsis
- Renal ischemia-reperfusion (IR) injury leads to acute kidney injury (AKI) through increased calcium influx and reactive oxygen species (ROS), causing necrosis and inflammation.
- Transient receptor potential (TRP) channels, including various types like TRPM, play roles in important cellular functions and are activated during IR injury.
- TRPM2 channels specifically contribute to renal damage during IR injury; mice lacking TRPM2 show resistance to this type of kidney damage.
Article Abstract
Renal ischemia-reperfusion (IR) injury triggers a cascade of signaling reactions involving an increase in Ca charge and reactive oxygen species (ROS) levels resulting in necrosis, inflammation, apoptosis, and subsequently acute kidney injury (AKI).Transient receptor potential (TRP) channels include an essential class of Ca permeable cation channels, which are segregated into six main channels: the canonical channel (TRPC), the vanilloid-related channel (TRPV), the melastatin-related channel (TRPM), the ankyrin-related channel (TRPA), the mucolipin-related channel (TRPML) and polycystin-related channel (TRPP) or polycystic kidney disease protein (PKD2). TRP channels are involved in adjusting vascular tone, vascular permeability, cell volume, proliferation, secretion, angiogenesis and apoptosis.TRPM channels include eight isoforms (TRPM1-TRPM8) and TRPM2 is the second member of this subfamily that has been expressed in various tissues and organs such as the brain, heart, kidney and lung. Renal TRPM2 channels have an important role in renal IR damage. So that TRPM2 deficient mice are resistant to renal IR injury. TRPM2 channels are triggered by several chemicals including hydrogen peroxide, Ca, and cyclic adenosine diphosphate (ADP) ribose (cADPR) that are generated during AKI caused by IR injury, as well as being implicated in cell death caused by oxidative stress, inflammation, and apoptosis.
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