Publication Name	World Journal of Diabetes
Manuscript ID	88354
Country	China

Category	Endocrinology & Metabolism
Manuscript Type	Basic Study
Article Title	Empagliflozin ameliorates diabetic cardiomyopathy probably via activating AMPK/PGC-1a and inhibiting the RhoA/ROCK pathway
Manuscript Source	Unsolicited Manuscript
All Author List	Na Li, Qiu-Xiao Zhu, Gui-Zhi Li, Ting Wang and Hong Zhou
Funding Agency and Grant Number	Funding Agency Grant Number Health Commission of Hebei Province 20210196 S＆T Program of Hebei 22377726D
Corresponding Author	Hong Zhou, PhD, Chief Physician, Doctor, Doctor, Department of Endocrinology, The Second Hospital of Hebei Medical University, No. 215, Heping West Road, Shijiazhuang 050000, Hebei Province, China. zhoubs2013@163.com
Key Words	Empagliflozin; Diabetic cardiomyopathy; AMPK; ROCK; Apoptosis; Oxidative stress
Core Tip	We established a diabetic cardiomyopathy model in db/db mice and treated the mice with empagliflozin for 8 wk, and found that empagliflozin observably improved cardiac function in diabetic mice, which was maybe related to activation of AMP-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1a) and inhibition of the RhoA/ROCK pathway. In order to exclude the effects of metabolic improvement on the heart in vivo, in vitro experiment in high glucose conditions was performed. The results confirmed that the anti-oxidative stress and anti-apoptotic effects of empagliflozin on cardiomyocytes were achieved by activating AMPK/PGC-1a and inhibiting ROCK. Furthermore, the effects were independent of sodium-glucose cotransporter (SGLT)2 inhibition as no SGLT2 expression was detected on cardiomyocytes.
Citation	Li N, Zhu QX, Li GZ, Wang T, Zhou H. Empagliflozin ameliorates diabetic cardiomyopathy probably via activating AMPK/PGC-1 and inhibiting the RhoA/ROCK pathway. World J Diabetes 2023; I14(12): 1862-1876

Received	2023-09-21 13:29
Peer-Review Started	2023-09-21 13:30
To Make the First Decision
Return for Revision	2023-10-10 08:48
Revised	2023-10-20 11:50
Second Decision	2023-11-14 01:15
Accepted by Journal Editor-in-Chief
Accepted by Executive Editor-in-Chief	2023-11-17 08:49
Articles in Press	2023-11-17 08:49
Publication Fee Transferred
Edit the Manuscript by Language Editor	2023-11-13 02:53
Typeset the Manuscript	2023-12-08 03:44

ISSN	1948-9358 (online)
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