SGLT2 Inhibitors Beyond Glycemic Control Toward Precision Therapy: A Narrative Review
Heart failure is a complicated syndrome with an array of causes which is associated with reduced cardiac function and highly heterogeneous treatment responses. Recently, there has been no clinical optimization of outcomes due to the intensive reliance on pharmacological therapies which further necessitates the development of personalized treatment approaches. Strides in HF medicine came with the advent of sodium-glucose co-transporter 2 inhibitors (SGLT2Is) such as Dapagliflozin, Empagliflozin and canagliflozin which have shown to be useful in HF due to its cardioprotective property beyond controlling glucose, reducing cardiovascular mortality, and hospitalization. However, it is well documented that responses to treatment with SGLT2Is are heterogeneous and this may be due to genetic polymorphisms affecting important pathways like cardiac function, inflammation, and fibrosis among others. This review explores the effects of SGLT2 inhibitors on cardiac remodeling in heart failure, focusing on left ventricular ejection fraction (LVEF), echocardiographic changes, and fibrosis biomarkers. The review will also highlight the importance of genetic testing in shaping clinical decisions and the management of HF. Such an effort may shift the treatment paradigm of HF patients and significantly improve their prognosis.
Authors
- Samar S. Azab (ORCID: https://orcid.org/0000-0002-0253-8280)
- Sara M. Shaheen (ORCID: https://orcid.org/0000-0001-5295-6926)
- Neven Sarhan (ORCID: https://orcid.org/0000-0002-4067-5518)
- Randa Mokhtar
- Ahmed Shawky (ORCID: https://orcid.org/0000-0002-3795-2422)
- Haidy E Michel
Institutions
- Ain Shams University (EG)
- Misr International University (EG)
Publication Details
- Journal
- Archives of Pharmaceutical Sciences Ain Shams University
- Published
- 2025-11-15
- DOI
- https://doi.org/10.21608/aps.2025.383494.1224
- Primary Topic
- Diabetes Treatment and Management
- Type
- article
- Field-Weighted Citation Impact
- 0.00