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Contusion concomitant with ischemia injury to skeletal muscles is common in civilian and battlefield trauma. Despite their clinical importance, few experimental studies on these injuries are reported. The present study established a rat skeletal muscle contusion concomitant with ischemia injury model to identify skeletal muscle alterations compared with contusion injury or ischemia injury. Macroscopic and microscopic morphological evaluation showed that contusion concomitant with ischemia injury aggravated muscle edema and hematoxylin-eosin (HE) injury score at 24 h postinjury. Serum creatine kinase (CK) and lactate dehydrogenase (LDH) levels, together with gastrocnemius muscle (GM) tumor necrosis factor-alpha (TNF-α) content elevated at 24 h postinjury too. During the 28-day follow-up, electrophysiological and contractile impairment was more severe in the contusion concomitant with ischemia injury group. In addition, contusion concomitant with ischemia injury decreased the percentage of larger (600-3000 μm) fibers and increased the fibrotic area and collagen I proportion in the GM. Smaller proportions of Pax7 and MyoD satellite cells (SCs) were observed in the contusion concomitant with ischemia injury group at 7 days postinjury. In conclusion, contusion concomitant with ischemia injury to skeletal muscle not only aggravates early muscle fiber necrosis but also hinders muscle functional recovery by impairing SC differentiation and exacerbating fibrosis during skeletal muscle repair.
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http://dx.doi.org/10.1177/15353702221102376 | DOI Listing |
J Cardiovasc Transl Res
September 2025
Department of Cardiology, Bei'an Hospital, Beidahuang Group, Heihe, 164000, Heilongjiang Province, China.
Myocardial ischemia/reperfusion injury (MIRI) worsens ischemic damage, with ferroptosis as a key mediator of this iron-dependent cell death. Lactylation, a novel epigenetic modification, remains poorly understood in MIRI-associated ferroptosis. This study aimed to elucidate the mechanistic link between lactylation and ferroptosis in MIRI.
View Article and Find Full Text PDFPediatr Cardiol
September 2025
Pediatric Cardiology Unit, University Hospital of Geneva, Geneva, Switzerland.
Anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA) is a rare congenital anomaly. Its clinical course is typically severe in infancy, leading to left ventricular ischemia, cardiogenic shock, and high mortality without surgical intervention.We describe a rare case of a 3-year-old girl diagnosed with ALCAPA, showing extensive right-to-left collaterals, preserved left ventricular function, and minimal myocardial injury.
View Article and Find Full Text PDFJ Biochem Mol Toxicol
September 2025
Department of Rehabilitation Medicine, Hebei Engineering University Affiliated Hospital, Handan, Hebei, China.
Blood-Brain Barrier (BBB) dysfunction acts as a key mediator of ischemic brain injury, contributing to brain edema, inflammatory cell infiltration, and neuronal damage. The integrity of the BBB is largely maintained by tight junction proteins, such as Claudin-5, and its disruption exacerbates neurological deficits. Neurokinin B (NKB), a neuropeptide that belongs to the tachykinin family, has been implicated in various physiological processes, including neuroinflammation and vascular function.
View Article and Find Full Text PDFJ Biochem Mol Toxicol
September 2025
Department of Anesthesiology, Qianjiang Maternal and Child Health and Family Planning Service Centre, Qianjiang, Hubei, China.
Acute lung injury (ALI) is a major contributor to the high morbidity and mortality associated with intestinal ischemia-reperfusion (II/R). Despite its severity, current clinical management of ALI remains limited to supportive care without addressing the cause of the disease, underscoring the urgent need to investigate the underlying mechanism and develop targeted therapies. In this study, we employed both in vitro and in vivo models to explore ALI in the setting of II/R.
View Article and Find Full Text PDFJ Integr Neurosci
August 2025
Department of Neurology, Peking University First Hospital Taiyuan Hospital, 030000 Taiyuan, Shanxi, China.
Background: Remote ischemic conditioning (RIC), a novel neuroprotective therapy, has broad potential for reducing the occurrence and recurrence of cerebrovascular events, yet its mechanisms are not incompletely understood. The aim of this study is to investigate whether RIC alleviates apoptosis, inflammation, and reperfusion injury in rat models of ischemic stroke by regulating the Elabela (ELA)-apelin-Apelin receptor (APJ) system.
Methods: We established a rat model of middle cerebral artery occlusion (MCAO) with ischemia-reperfusion injury, and RIC was administered twice daily for 3 days post-MCAO.