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Hypoxic myocardial injury is the core mechanism of many cardiovascular diseases and poses a serious threat to global public health. Its pathogenesis involves energy metabolism disorder, oxidative stress, inflammatory response, apoptosis regulation imbalance, and other links, resulting in myocardial dysfunction and damage. In recent years, a large number of studies have confirmed that the Toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) signaling network can regulate hypoxic myocardial injury by mediating HMGB1, MyD88, Caspase-3, HIF-1α, TNF-α, NLRP3, HSP70, etc. Traditional Chinese Medicine (TCM) and its active components have obvious advantages in the treatment of complex diseases such as hypoxic myocardial injury, and inhibiting the key target of TLR4/NF-κB signaling network is one of the mechanisms of myocardial protection. However, there are few systematic reviews and summaries in this field. Based on this, this review summarizes the regulatory mechanism of TLR4/NF-κB signaling pathway involved in hypoxic myocardial injury and the intervention effect of TCM in recent years, to provide a theoretical basis for basic research and new drug development of hypoxic myocardial injury.
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http://dx.doi.org/10.1016/j.fitote.2025.106721 | DOI Listing |
Gen Physiol Biophys
September 2025
Department of Cardiology, The Fourth Affiliated Hospital of Harbin Medical University, Nangang District, Harbin, Heilongjiang, China.
Exosomes derived from various cells have been demonstrated to contribute to cardiac repair by regulating macrophage polarization in myocardial infarction. However, how exosomes secreted from cardiomyocytes under hypoxia-ischemia (Hypo-Exo) regulate macrophage polarization in the local tissues is elusive. This study aimed to determine the underlying mechanisms by which Hypo-Exo polarized M2 macrophages.
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September 2025
National Heart Center Singapore, Singapore, Singapore.
Cardiovascular diseases are increasingly recognized as chronic disorders driven by a complex interplay between inflammation and fibrosis. In this review, we elucidate emerging mechanisms that govern the transition from acute inflammation to pathological fibrosis, with particular focus on cellular crosstalk between neutrophils, macrophages, fibroblasts, and myofibroblasts. We explore how dysregulated immune responses and extracellular matrix (ECM) remodeling sustain a pathogenic feedback loop, promoting myocardial stiffening and adverse cardiac remodeling.
View Article and Find Full Text PDFJ 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 PDFCardiovasc Ther
September 2025
Department of Cardiac Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.
Yes-associated protein (YAP) is a major downstream nuclear coactivator of the Hippo pathway and is activated during myocardial hypertrophy. Verteporfin, a YAP inhibitor, may serve as a potential treatment for myocardial hypertrophy. This study was aimed at exploring the role and underlying mechanisms of verteporfin in isoproterenol (ISO)-induced myocardial hypertrophy both in vivo and in vitro.
View Article and Find Full Text PDFFront Cardiovasc Med
August 2025
The First Hospital of Nanchang, The Third Affiliated Hospital of Nanchang University, Nanchang University, Nanchang, Jiangxi, China.
tRNA-derived small RNAs (tsRNAs) are a class of non-coding RNAs that are generated by cleavage of precursors or mature tRNAs under stress conditions such as hypoxia, oxidative stress and nutrient deficiency. Recent breakthroughs in RNA sequencing technology have revealed their association with cardiovascular diseases (CVDs), including myocardial infarction (MI), atherosclerosis, cardiac hypertrophy, aortic coarctation, and pulmonary arterial hypertension. tsRNAs play important biological functions in these diseases, including the inhibition of apoptosis, epigenetic modification, intercellular signaling mediation, translation, and regulation of gene expression.
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