![]() The critical roles of mitochondria in cardiac ischemia-reperfusion injury, acute myocardial infarction, atherosclerosis, and cardiac aging have recently been reviewed detailedly ( 9– 12). Therefore, mitochondria serve as the central organelle responsible for coordinating the energy transduction and maintaining the contractile performance of CMs. It is also estimated that 60–90% of the energy adult hearts required is originated from the oxidation of fatty acid in mitochondria ( 8). Morphometry analysis has demonstrated that the contents of mitochondria occupy 22.0-37.0% of the CMs' mass in various species, and most importantly, the volume densities of mitochondria are closely related to heart rate and cardiac oxygen consumption rate ( 7). It is widely accepted that mitochondria serve as the power-house of cells and mitochondrial dysfunction often highly correlates with cell pathology, especially in cells requiring high-energy supply such as CMs. With the continuous deepening of research and updating of knowledge, energy metabolism has shown an increasingly compelling role in cardiac hypertrophy. Over the past few decades,extensive studies have established that previously unrecognized mechanisms, including epigenetic modifications, immunomodulation, impaired protein quality control, aberrant Ca2+ handling, metabolic reprogramming, and cell-to-cell interactions, are involved in the initiation and progression of cardiac hypertrophy ( 5). It is well established that pathological cardiac hypertrophy has become an independent risk factor for the development of heart failure (HF), a major and growing public health problem globally with increasing morbidity, high mortality, and heavy economic burdens ( 6). Pressure/volume overload, Angiotensin II (Ang II), oxidants, activation of α/β adrenergic receptors, hypoxia, aging, and high-glucose are efficient inducers of pathological cardiac hypertrophy ( 5). In contrast, pathological hypertrophy, a decompensated stage with complex network of cellular and molecular regulation, usually observed in patients with long-term cardiovascular disorders, is accompanied by cardiac systolic/diastolic dysfunction and the enlargement of CMs is often irreversible ( 3, 4). ![]() ![]() Physiological hypertrophy, which usually occurs during pregnancy and exercise, is characterize with a coordinated increase in ventricular volume and wall thickness, most importantly, it is reversible once the stimulus was relieved ( 2). Cardiac hypertrophy can be generally divided into physiological and pathological hypertrophy. Therefore, in adult hearts, CMs have no capability of proliferating in response to prolonged pressure/volume overload instead, they exhibit morphological enlargement to continuously pump blood to provide oxygen and nutrients to the body, thus leading to the increased heart wall thickness and heart mass, and eventually cardiac hypertrophy ( 1). Our article is also to summarize the strategies of mitochondria-targeting as therapeutic targets to treat cardiac hypertrophy.Ĭardiomyocytes (CMs) are one of the most important cell types which become terminally differentiated once after birth. This article presents a summary review of the morphological and functional changes of mitochondria during the hypertrophic response, followed by an overview of the latest research progress on the significant modulatory roles of mitochondria in cardiac hypertrophy. ![]() The significant alterations in mitochondrial energetics and mitochondrial proteome composition, as well as the altered expression of transcripts that have an impact on mitochondrial structure and function, may contribute to the initiation and progression of cardiac hypertrophy. In recent years, accumulating evidence has indicated that mitochondrial dysfunction is implicated in pathological cardiac hypertrophy. Sustained cardiac overload inevitably results in high energy consumption, thus breaking the balance between mitochondrial energy supply and cardiac energy demand. ![]() 3Department of Thyroid and Breast, Renmin Hospital of Wuhan University, Wuhan, ChinaĬardiac hypertrophy, a stereotypic cardiac response to increased workload, ultimately progresses to severe contractile dysfunction and uncompensated heart failure without appropriate intervention.2Hubei Key Laboratory of Metabolic and Chronic Diseases, Wuhan, China.1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.Dan Yang 1,2 †, Han-Qing Liu 3 †, Fang-Yuan Liu 1,2, Zhen Guo 1,2, Peng An 1,2, Ming-Yu Wang 1,2, Zheng Yang 1,2, Di Fan 1,2 * and Qi-Zhu Tang 1,2 * ![]()
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