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Potential Protective Mechanism in the Cardiac Microvascular Injury
Xiuchuan Li1,2, Juanni Hou1,2, Jin Du1,2
1From the Graduate School, Third Military Medical University, Chongqing, China (X.L., J.H., J.D., H.P., Y.Y.).
Hypertension (Dallas, Tex. : 1979)
|May 9, 2018
Summary
Type 2 diabetes mellitus (T2DM) impairs cardiac microvessels by reducing TRPV1 expression, increasing oxidative stress. Capsaicin protects against T2DM-induced injury by restoring the TRPV1 pathway.
Area of Science:
- Cardiovascular Biology
- Endocrinology
- Molecular Medicine
Background:
- Type 2 diabetes mellitus (T2DM) is associated with cardiac microvascular injury, characterized by hyperglycemia and hyperlipidemia.
- The role of transient receptor potential vanilloid 1 (TRPV1) in cardiac microvessels during T2DM remains unclear, despite its complex involvement in other cardiac conditions.
Purpose of the Study:
- To elucidate the specific function of TRPV1 in cardiac microvascular endothelial cells (CMECs) within the context of T2DM.
- To investigate the molecular mechanisms underlying T2DM-induced cardiac microvascular damage and the potential protective effects of TRPV1 modulation.
Main Methods:
- Established T2DM mouse models using streptozotocin and high-fat feeding.
- Cultured CMECs under normal glucose, high glucose (HG), high fatty acid (HF), and combined HG-HF conditions.
- Assessed TRPV1 expression, intracellular calcium ([Ca2+]i), apoptosis, nitric oxide (NO) production, reactive oxygen species (ROS), nitrotyrosine, PGC-1α, and OPA1 levels. Utilized TRPV1 knockout (TRPV1-/-) models and capsaicin treatment.
Main Results:
- High glucose and high fatty acids (HG-HF) significantly inhibited TRPV1 expression and reduced [Ca2+]i in CMECs.
- T2DM exacerbated cardiac dysfunction, impaired glucose uptake, and damaged the microvascular barrier, effects amplified in TRPV1-/- models.
- HG-HF exposure, especially in TRPV1-/- CMECs, increased apoptosis, decreased NO production, and elevated ROS and nitrotyrosine.
- TRPV1 deficiency worsened HG-HF-induced suppression of PGC-1α and OPA1, with OPA1 supplementation showing partial reversal.
- Capsaicin treatment attenuated HG-HF-induced CMEC injury and mitigated T2DM-related cardiac microvascular damage.
Conclusions:
- T2DM induces cardiac microvascular injury through a detrimental cycle of TRPV1 inhibition and excessive reactive oxygen species.
- TRPV1 plays a crucial protective role in CMECs against T2DM-induced oxidative and nitrative stress.
- Long-term capsaicin administration offers cardioprotection in T2DM by targeting the TRPV1/Ca2+/PGC-1α/OPA1 pathway, suppressing oxidative stress.
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