Calcium homeostasis plays an essential role in maintaining excitation-contraction coupling (ECC) in cardiomyocytes, including calcium release, recapture, and storage. Disruption of calcium homeostasis may affect heart function, leading to the development of various heart diseases. Myocardial ischemia/reperfusion (MI/R) injury may occur after revascularization, which is a treatment used in coronary heart disease. MI/R injury is a complex pathological process, and the main cause of increased mortality and disability after treatment of coronary heart disease. However, current methods and drugs for treating MI/R injury are very scarce, not ideal, and have limitations. Studies have shown that MI/R injury can cause calcium overload that can further aggravate MI/R injury. Therefore, we reviewed the effects of critical calcium pathway regulators on MI/R injury and drew an intuitive diagram of the calcium homeostasis pathway. We also summarized and analyzed calcium pathway-related or MI/R drugs under research or marketing by searching Therapeutic Target and PubMed Databases. The data analysis showed that six drugs and corresponding targets are used to treat MI/R injury and involved in calcium signaling pathways. We emphasize the relevance of further detailed investigation of MI/R injury and calcium homeostasis and the therapeutic role of calcium homeostasis in MI/R injury, which bridges basic research and clinical applications of MI/R injury.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7296066PMC
http://dx.doi.org/10.3389/fphar.2020.00872DOI Listing

Publication Analysis

Top Keywords

mi/r injury
40
calcium homeostasis
24
injury
11
mi/r
11
calcium
10
myocardial ischemia/reperfusion
8
treatment coronary
8
coronary heart
8
heart disease
8
injury calcium
8

Similar Publications

Interleukin-34 (IL-34) was recently reported to be a new biomarker for atherosclerosis diseases, such as coronary artery disease and vascular dementia. IL-34 regulates the expression of proinflammatory cytokines (IL-17A, IL-1 and IL-6), which are classical cytokines involved in myocardial ischemia‒reperfusion (MI/R) injury. However, the exact role of IL-34 in MI/R remains unknown.

View Article and Find Full Text PDF

ROS-differentiated release of Apelin-13 from hydrogel comprehensively treats myocardial ischemia-reperfusion injury.

J Control Release

January 2025

Department of Cardiology, Zhongda Hospital, School of Medicine, Southeast University, 87 Dingjiaqiao, Nanjing 210009, China. Electronic address:

Treatment of myocardial ischemia-reperfusion (MI/R) injury still faces the lack of clinically approved drugs. Apelin-13 is a highly promising drug candidate of MI/R injury, but hampered by its extremely short half-life in plasma. This calls for efficient and smart delivering system for Apelin-13 delivery, but has not been reported.

View Article and Find Full Text PDF

Ropivacaine and celecoxib-loaded injectable composite hydrogel for improved chronic pain-exacerbated myocardial ischemia-reperfusion injury.

J Control Release

January 2025

Department of Joint and Orthopedics, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, PR China. Electronic address:

Chronic pain is a prevalent condition affecting a significant portion of the global population and is known to be associated with an increased risk of cardiovascular diseases. Despite the clinical relevance, the mechanisms underlying the link between chronic pain and myocardial ischemia-reperfusion (MI/R) injury remain poorly understood. This study aimed to investigate the role of the superior cervical ganglion (SCG) in mediating the effects of chronic pain on MI/R injury and to develop a novel therapeutic strategy.

View Article and Find Full Text PDF

Arachidonic acid synergizes with aspirin preventing myocardial ischemia-reperfusion injury and mitigates bleeding risk.

Cardiovasc Res

January 2025

State Key Laboratory of Cardiovascular Disease, Clinical Pharmacology Center, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100037, China.

Aims: The therapeutic efficacy of coronary revascularization is compromised by myocardial ischemia-reperfusion (MI/R) injury. Higher levels of circulating arachidonic acid (AA) are reportedly associated with lower risk of cardiovascular disease. The cyclooxygenase (COX) pathway metabolizes AA into prostaglandins (PGs) and the platelet-activating thromboxane A2 (TXA2), which is inhibited by aspirin.

View Article and Find Full Text PDF

Adipocyte-derived small extracellular vesicles exacerbate diabetic ischemic heart injury by promoting oxidative stress and mitochondrial-mediated cardiomyocyte apoptosis.

Redox Biol

February 2025

Department of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA, USA; Department of Biomedical Engineering, UAB, Birmingham, AL, USA. Electronic address:

Background: Diabetes increases ischemic heart injury via incompletely understood mechanisms. We recently reported that diabetic adipocytes-derived small extracellular vesicles (sEV) exacerbate myocardial reperfusion (MI/R) injury by promoting cardiomyocyte apoptosis. Combining in vitro mechanistic investigation and in vivo proof-concept demonstration, we determined the underlying molecular mechanism responsible for diabetic sEV-induced cardiomyocyte apoptosis after MI/R.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!