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Article

Subacute Hypoxia Induces Cardiac Remodeling and Mitochondrial Dysfunction via Apoptotic Pathways in a Rabbit Model of Tracheal Stenosis

by
Taeyun Kim
1,
Kyoung-Im Cho
1,
Hyoung Kyu Kim
2,*,
Chulho Oak
1,*,
Jin Han
2,
Hyoung Shin Lee
3 and
Yohan Jeon
4
1
Department of Internal Medicine, Kosin University College of Medicine, Busan 49267, Republic of Korea
2
Basic Research Laboratory, Cardiovascular and Metabolic Disease Core Research Support Center, Inje University, Busan 47329, Republic of Korea
3
Department of Otolaryngology-Head and Neck Surgery, Kosin University College of Medicine, Busan 49267, Republic of Korea
4
Department of Pathology, Kosin University College of Medicine, Busan 49267, Republic of Korea
*
Authors to whom correspondence should be addressed.
J. Cardiovasc. Dev. Dis. 2025, 12(10), 377; https://doi.org/10.3390/jcdd12100377
Submission received: 7 August 2025 / Revised: 22 September 2025 / Accepted: 23 September 2025 / Published: 24 September 2025
(This article belongs to the Section Acquired Cardiovascular Disease)
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Abstract

Myocardial hypoxia is a major cause of cardiac dysfunction, triggering cellular injury and apoptosis. This study aims to investigate the effects of subacute hypoxia on cardiac remodeling and mitochondrial oxygen consumption. This study is based on a rabbit experimental model. Hypoxia was induced using a rabbit tracheal stenosis model. Endotracheal intubation with a 1.5 cm segmented tube wrapped with an absorbable hemostat was used to generate tracheal stenosis in six rabbits. Sham controls (n = 3) underwent tracheotomy, with the tracheal exposure site being sutured immediately. After 1 week, the tube was removed. Echocardiography and mitochondrial function from both groups were morphologically and functionally analyzed at 2 weeks after endoscopic confirmation of tracheal stenosis. Compared to sham group, tracheal stenosis group showed significantly reduced interventricular septal wall thickness (2.3 ± 0.1 mm vs. 2.7 ± 0.2 mm, p = 0.08) and enlarged left ventricular end-diastolic volume (5.86 ± 0.58 mL vs. 5.39 ± 0.18 mL, p = 0.46) with reduced left ventricular ejection fraction (54.5 ± 5.3% vs. 66.9 ± 4.0%, p = 0.005). The tracheal stenosis group showed significantly reduced mitochondrial oxygen consumption at state 3 with reduced respiratory control ratio. Caspase activities (caspase-9 and caspase-3) were increased in the tracheal stenosis group than in the sham group. Subacute hypoxia induced by the tracheal stenosis model causes cardiac remodeling and mitochondrial dysfunction through apoptotic pathways. This study suggests that management of hypoxia could prevent cellular apoptosis and cardiac dysfunction.
Keywords: tracheal stenosis; hypoxia; cardiac remodeling; mitochondria; apoptosis tracheal stenosis; hypoxia; cardiac remodeling; mitochondria; apoptosis

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MDPI and ACS Style

Kim, T.; Cho, K.-I.; Kim, H.K.; Oak, C.; Han, J.; Lee, H.S.; Jeon, Y. Subacute Hypoxia Induces Cardiac Remodeling and Mitochondrial Dysfunction via Apoptotic Pathways in a Rabbit Model of Tracheal Stenosis. J. Cardiovasc. Dev. Dis. 2025, 12, 377. https://doi.org/10.3390/jcdd12100377

AMA Style

Kim T, Cho K-I, Kim HK, Oak C, Han J, Lee HS, Jeon Y. Subacute Hypoxia Induces Cardiac Remodeling and Mitochondrial Dysfunction via Apoptotic Pathways in a Rabbit Model of Tracheal Stenosis. Journal of Cardiovascular Development and Disease. 2025; 12(10):377. https://doi.org/10.3390/jcdd12100377

Chicago/Turabian Style

Kim, Taeyun, Kyoung-Im Cho, Hyoung Kyu Kim, Chulho Oak, Jin Han, Hyoung Shin Lee, and Yohan Jeon. 2025. "Subacute Hypoxia Induces Cardiac Remodeling and Mitochondrial Dysfunction via Apoptotic Pathways in a Rabbit Model of Tracheal Stenosis" Journal of Cardiovascular Development and Disease 12, no. 10: 377. https://doi.org/10.3390/jcdd12100377

APA Style

Kim, T., Cho, K.-I., Kim, H. K., Oak, C., Han, J., Lee, H. S., & Jeon, Y. (2025). Subacute Hypoxia Induces Cardiac Remodeling and Mitochondrial Dysfunction via Apoptotic Pathways in a Rabbit Model of Tracheal Stenosis. Journal of Cardiovascular Development and Disease, 12(10), 377. https://doi.org/10.3390/jcdd12100377

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