The past few decades have witnessed an enormous number of research strategies aimed at protecting the heart against myocardial ischemia-reperfusion injury. Several randomized clinical trials are nowadays in progress testing whether promising therapeutic strategies aimed at preventing lethal reperfusion injury can be translated from bench to bedside. Many of these interventions, either pharmacological or mechanical, are targeting mitochondria as the final effectors of cardioprotection. Despite encouraging pre-clinical studies and small proof of concept clinical trials, there are still several limitations that may jeopardize the efficacy of cardioprotective strategies. These limitations include clinical setting, patient profile, drug administration, and methods for evaluating treatment efficacy. Identifying potential mechanistic and methodological pitfalls in the field may improve future translational research.
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http://dx.doi.org/10.1139/cjpp-2013-0048 | DOI Listing |
Front Endocrinol (Lausanne)
January 2025
Clinical Studies Group, Randox Laboratories Ltd, Crumlin, United Kingdom.
Background: In patients undergoing orthopaedic trauma surgery, acute kidney injury (AKI) can develop post-operatively and is a major cause of increased mortality and hospital stay time. Development of AKI is associated with three main processes: inflammation, ischaemia-reperfusion injury (IRI) and hypoperfusion. In this study, we investigated whether ratios of urine and blood anti-inflammatory biomarkers and biomarkers of hypoperfusion, IRI and inflammation are elevated in patients who develop post-trauma orthopaedic surgery acute kidney injury (PTOS-AKI).
View Article and Find Full Text PDFBMC Complement Med Ther
January 2025
Institute of Basic Medical Sciences of Xiyuan Hospital, Beijing Key Laboratory of Chinese Materia Pharmacology, China Academy of Chinese Medical Sciences, National Clinical Research Center of Traditional Chinese Medicine for Cardiovascular Diseases, Beijing, China.
Objectives: This study intended to explore whether the protective effect safflower yellow injection (SYI) on myocardial ischemia-reperfusion (I/R) injury in rats mediated of the NLRP3 inflammasome signaling.
Methods: The I/R model was prepared by ligating the left anterior descending coronary artery for 45 min and then releasing the blood flow for 150 min. 96 male Wistar rats were randomly divided into sham group, I/R group, Hebeishuang group (HBS), SYI high-dose group (I/R + SYI-H), SYI medium-dose group (I/R + SYI-M) and SYI low-dose group (I/R + SYI-L).
Sci Rep
January 2025
Center for Engineering in Medicine and Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Static cold storage of donor livers at 4 °C incompletely arrests metabolism, ultimately leading to decreases in ATP levels, oxidative stress, cell death, and organ failure. Hydrogen Sulfide (HS) is an endogenously produced gas, previously demonstrated to reduce oxidative stress, reduce ATP depletion, and protect from ischemia and reperfusion injury. HS is difficult to administer due to its rapid release curve, resulting in cellular death at high concentrations.
View Article and Find Full Text PDFBrain Res Bull
January 2025
Department of Joint, Honghui Hospital, Xi'an Jiaotong University, No.555 Youyi East Road, Xi'an City, Shaanxi Province, 710054, PR China. Electronic address:
Background: Electroacupuncture (EA) and trigonelline (TG) have been reported to be beneficial in alleviating cerebral ischemia/reperfusion injury (CIRI). However, the synergistic effects of EA and TG in CIRI and the underlying mechanism have not been demonstrated.
Methods: Rats were subjected to middle cerebral artery occlusion (MCAO) surgery and reperfusion (MCAO/R) to establish a CIRI model.
Cell Metab
January 2025
Cardiovascular and Metabolic Diseases, Duke-NUS Medical School, Singapore, Singapore. Electronic address:
Mitochondrial electron transport chain (ETC) complexes partition between free complexes and quaternary assemblies known as supercomplexes (SCs). However, the physiological requirement for SCs and the mechanisms regulating their formation remain controversial. Here, we show that genetic perturbations in mammalian ETC complex III (CIII) biogenesis stimulate the formation of a specialized extra-large SC (SC-XL) with a structure of I+III, resolved at 3.
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