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Biomedicines
Volume 14
Issue 7
10.3390/biomedicines14071445
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This is an early access version, the complete PDF, HTML, and XML versions will be available soon.
Article

Isoproterenol Induces Cardiac Injury and Senescence in Sprague–Dawley Rats: A Cost-Effective Pharmacological Model

by
Ahmed Altuwaijri
1,*,
Sarah M. Almufadhili
1,
Taher Hashim Almaki
2,
Dalal Alkhelb
1,
Sultan Almudimeegh
1,
Faris Almutairi
1,
Abdulaziz M. S. Alsaad
1 and
Homood M. As Sobeai
1
1
Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia
2
The Pharmaceutical Care Department, Al Kharj Armed Forces Hospitals, Al-Kharj 16294, Saudi Arabia
*
Author to whom correspondence should be addressed.
Biomedicines 2026, 14(7), 1445; https://doi.org/10.3390/biomedicines14071445 (registering DOI)
Submission received: 19 May 2026 / Revised: 10 June 2026 / Accepted: 23 June 2026 / Published: 25 June 2026
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Cardiovascular Diseases: 2nd Edition)
Review Reports Versions Notes

Abstract

Background/Objectives: Cardiovascular disease increases with ageing and remains the leading cause of death worldwide. Cellular senescence contributes to cardiac dysfunction in the older population by secreting the senescence-associated secretory phenotype (SASP). Cardiac injury models induced by surgery have been shown to induce senescence in young adult rodents. However, surgical models are complex and associated with high mortality. Methods: We established a rat model of injury and senescence using isoproterenol (ISO). Male SD rats received ISO (100 mg/kg) for five days, then hearts were collected on days 10 and 28 after the first ISO dose. Results: ISO administration caused cardiac injury, manifested by inflammatory infiltration, fibrosis, and increased cardiomyocyte cross-sectional area. Cardiac injury was accompanied by an increase in the senescence markers SA-β-gal, p16 and p21, and DNA damage marker γH2AX. Moreover, the mRNA levels of p21 increased on day 10, along with several SASP factors, whereas the mRNA levels of p16 increased on day 28. Fibrosis, hypertrophy, and senescence persisted until day 28, indicating long-lasting cardiac remodeling and senescent cell accumulation. Conclusions: These findings suggest that ISO can provide a simple, cost-effective platform for studying senescence and cardiac injury. This model facilitates the study of timing, dosage, mechanisms and efficacy of senolytic interventions and may contribute to the development of senescence-targeted therapies.
Keywords: cardiac injury; cellular senescence; cardiac remodeling; senolytics; isoproterenol; ageing cardiac injury; cellular senescence; cardiac remodeling; senolytics; isoproterenol; ageing

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MDPI and ACS Style

Altuwaijri, A.; Almufadhili, S.M.; Almaki, T.H.; Alkhelb, D.; Almudimeegh, S.; Almutairi, F.; Alsaad, A.M.S.; As Sobeai, H.M. Isoproterenol Induces Cardiac Injury and Senescence in Sprague–Dawley Rats: A Cost-Effective Pharmacological Model. Biomedicines 2026, 14, 1445. https://doi.org/10.3390/biomedicines14071445

AMA Style

Altuwaijri A, Almufadhili SM, Almaki TH, Alkhelb D, Almudimeegh S, Almutairi F, Alsaad AMS, As Sobeai HM. Isoproterenol Induces Cardiac Injury and Senescence in Sprague–Dawley Rats: A Cost-Effective Pharmacological Model. Biomedicines. 2026; 14(7):1445. https://doi.org/10.3390/biomedicines14071445

Chicago/Turabian Style

Altuwaijri, Ahmed, Sarah M. Almufadhili, Taher Hashim Almaki, Dalal Alkhelb, Sultan Almudimeegh, Faris Almutairi, Abdulaziz M. S. Alsaad, and Homood M. As Sobeai. 2026. "Isoproterenol Induces Cardiac Injury and Senescence in Sprague–Dawley Rats: A Cost-Effective Pharmacological Model" Biomedicines 14, no. 7: 1445. https://doi.org/10.3390/biomedicines14071445

APA Style

Altuwaijri, A., Almufadhili, S. M., Almaki, T. H., Alkhelb, D., Almudimeegh, S., Almutairi, F., Alsaad, A. M. S., & As Sobeai, H. M. (2026). Isoproterenol Induces Cardiac Injury and Senescence in Sprague–Dawley Rats: A Cost-Effective Pharmacological Model. Biomedicines, 14(7), 1445. https://doi.org/10.3390/biomedicines14071445

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