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Mst1 inhibits CMECs autophagy and participates in the development of diabetic coronary microvascular dysfunction

Jie Lin1,2, Lei Zhang3, Mingming Zhang1,2

  • 1Department of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.

Scientific Reports
|September 30, 2016
PubMed

Insights

Mst1 knockout preserves cardiac microvessel integrity and improves cardiac function in diabetic mice by enhancing autophagy and reducing apoptosis in cardiac microvascular endothelial cells.

Area of Science:

  • Cardiovascular Biology
  • Cellular Metabolism
  • Diabetic Complications

Background:

  • Diabetic patients face significant cardiovascular morbidity and mortality.
  • Cardiac microvascular endothelial cell (CMEC) dysfunction is critical in diabetic coronary microvascular dysfunction.
  • Understanding molecular mechanisms is key to treating diabetic heart complications.

Purpose of the Study:

  • To investigate the role of Mst1 in diabetic coronary microvascular dysfunction.
  • To elucidate the impact of Mst1 on CMEC autophagy, apoptosis, and integrity.
  • To explore the relationship between Mst1, Sirt1, and diabetic cardiac complications.

Main Methods:

  • Constructed experimental diabetes models using Mst1 transgenic, Mst1 knockout, and sirt1 knockout mice.
  • Assessed cardiac microvessel integrity and cardiac function in vivo.
  • Evaluated CMEC autophagy and apoptosis under high glucose conditions in vitro.
  • Utilized Western blotting for LC3 expression and observed autophagosomes.

Main Results:

  • Mst1 overexpression in transgenic mice impaired cardiac microvessel integrity and function.
  • Mst1 knockout improved cardiac microvessel integrity and function in diabetic mice.
  • Mst1 inhibited CMEC autophagy and promoted apoptosis; Mst1 knockdown reversed these effects.
  • Sirt1 knockout counteracted the detrimental effects of Mst1 overexpression.

Conclusions:

  • Mst1 knockout protects against diabetic coronary microvascular dysfunction.
  • Mst1 exacerbates diabetic cardiac complications by reducing Sirt1 activity, inhibiting autophagy, and increasing CMEC apoptosis.
  • Targeting Mst1 may offer a therapeutic strategy for diabetic cardiovascular disease.

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