Results 201 to 210 of about 340,285 (357)

Expression of Neuronal Nitric Oxide Synthase (nNOS) on Ischemia/reperfusion Injury in Rat Spinal Cord [PDF]

open access: bronze, 2007
Hee Uk Kwon   +6 more
openalex   +1 more source

Interventional therapies for chronic heart failure: An overview of recent developments

open access: yesESC Heart Failure, Volume 12, Issue 2, Page 1081-1094, April 2025.
Abstract Heart failure (HF), the final manifestation of most cardiovascular diseases, has become a major global health concern, affecting millions of individuals. Despite basic drug treatments, patients present with high morbidity and mortality rates. However, recent advancements in interventional therapy have shown promising results in improving the ...
Bingchen Guo   +7 more
wiley   +1 more source

Ischemia Reperfusion Injury

open access: yesJACC: Basic to Translational Science, 2023
Gonzalo Pizarro, MD, PhD
doaj   +1 more source

PANoptosis and mitochondrial regulatory mechanisms in cerebral ischemia-reperfusion injury. [PDF]

open access: yesFront Physiol
Li L   +11 more
europepmc   +1 more source

Biochemical and Histopathologic Investigation of the Effect of Rilmenidine on Ovarian Ischemia-Reperfusion Injury in Rats [PDF]

open access: hybrid
Betül Kalkan Yılmaz   +8 more
openalex   +1 more source

Transendocardial injection of expanded autologous CD34+ cells after myocardial infarction: Design of the EXCELLENT trial

open access: yesESC Heart Failure, Volume 12, Issue 2, Page 1455-1463, April 2025.
Abstract Aims The extent of irreversible cardiomyocyte necrosis after acute myocardial infarction (AMI) is a major determinant of residual left ventricular (LV) function and clinical outcome. Cell therapy based on CD34+ cells has emerged as an option to help repair the myocardium and to improve outcomes.
Jerome Roncalli   +17 more
wiley   +1 more source

Metabolic abnormalities and reprogramming in cats with naturally occurring hypertrophic cardiomyopathy

open access: yesESC Heart Failure, Volume 12, Issue 2, Page 1256-1270, April 2025.
Abstract Background and aims The heart is a metabolic organ rich in mitochondria. The failing heart reprograms to utilize different energy substrates, which increase its oxygen consumption. These adaptive changes contribute to increased oxidative stress.
Qinghong Li   +12 more
wiley   +1 more source

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