BASIC RESEARCH IN CARDIOLOGY心血管基础研究
BASIC RESEARCH IN CARDIOLOGY(英文缩写 BASIC RES CARDIOL),ISSN 0300-8428,eISSN 1435-1803,中文译名:心血管基础研究 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 12.416 | Q1 |
| 2022 | 9.500 | Q1 |
| 2023 | 7.500 | Q1 |
| 2024 | 8.000 | Q1 |
| 2025 | 9.200 | Q1 |
BASIC RESEARCH IN CARDIOLOGY 最新收录文献
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1. Spinal neuronal TLR4-induced enhancement of nociceptive signals contributes to myocardial ischemia/reperfusion injury.
1. 脊髓神经元TLR4诱导的伤害性信号增强促进心肌缺血/再灌注损伤PMID:日期:2026-10-01Myocardial ischemia/reperfusion (I/R) injury has been extensively studied, yet the underlying neuroinflammatory mechanisms are not fully understood. While toll-like receptor 4 (TLR4) is known to be involved in neuropathic pain and neurodegeneration, its role in the central nervous system during myocardial I/R injury, as well as how it modulates neuronal activity to influence cardiac function, remains unclear. In this study, we established a rodent model of myocardial I/R injury by ligating the left anterior descending artery. We found that myocardial I/R injury significantly upregulated TLR4 expression in the spinal dorsal horn, with enhanced TLR4 levels predominantly localized to spinal neurons rather than astrocytes or microglia. Upregulation of TLR4 exhibited functional crosstalk with the calcitonin gene-related peptide (CGRP) receptor, facilitating the transmission of nociceptive signals from the injured myocardium and leading to hyperexcitation of spinal neurons. Both pharmacological inhibition and genetic manipulation of TLR4 signaling resulted in a marked reduction in neuronal activity and attenuated myocardial ischemic injury, accompanied by decreased nociceptive input from the heart to the spinal dorsal horn. Collectively, our findings reveal classic neuroinflammatory signals derived from TLR4 that contribute to neuronal hyperexcitation following myocardial I/R injury. Targeting spinal neuronal TLR4 signaling represents a promising therapeutic strategy for patients with acute myocardial injury.
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2. Short-chain fatty acids promote post-myocardial infarction cardiac repair via FFAR2-dependent suppression of osteoclast-like macrophage differentiation.
PMID:日期:2026-09-21Adverse cardiac remodeling leads to the development of heart failure following myocardial infarction (MI), yet the immunometabolic signals governing early infarct repair remain poorly understood. Short-chain fatty acids (SCFAs) are important immunometabolic regulators, but their relevance and mechanistic contribution to post-MI repair remain unclear. Here, we integrated clinical observations with genetic and pharmacological intervention studies to investigate the role of the SCFAs-free fatty acid receptor 2 (FFAR2) axis in post-MI repair. Circulating SCFAs levels were markedly decreased in patients with MI, and associated with more complex coronary lesions and a higher risk of major adverse cardiovascular events. In murine MI, SCFAs supplementation reduced infarct expansion, cardiomyocyte death, and cardiac rupture, and improved left-ventricular function. These benefits were lost in global and myeloid-specific Ffar2-deficient mice, demonstrating an essential role for myeloid FFAR2 in SCFA-mediated cardioprotection. Mechanistically, SCFAs activated FFAR2-G signaling in macrophages to suppress RANKL-RANK-driven osteoclast-like macrophage differentiation. thereby enhancing early fibrotic stabilization, reducing cardiomyocyte apoptosis, and improving infarct healing. Pharmacological blockade of osteoclast-like macrophage activation partially rescued impaired healing and cardiac dysfunction in myeloid-specific Ffar2-deficient mice after MI. These findings identify circulating SCFAs as clinically relevant biomarkers associated with coronary lesion complexity and adverse clinical outcomes after MI, and establish the SCFAs-FFAR2 axis as an immune-metabolic pathway that orchestrates macrophage fate and infarct healing. Targeting SCFAs-FFAR2 signaling may represent a therapeutic strategy to limit adverse post-MI remodeling and prevent heart failure.
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3. Enhanced myelopoiesis and myeloid TREM1 upregulation link obesity with adverse outcomes after myocardial infarction.
3. 增强的髓系生成和髓系TREM1上调将肥胖与心肌梗死后不良结局相关联PMID:日期:2026-09-11Obesity induces a systemic low-grade inflammatory activation of the innate immune system potentially impairing early outcomes after myocardial infarction (MI). This study aims to analyse the impact of diet-induced obesity on myelopoiesis, myocardial inflammation, left ventricular function and survival in an experimental mouse model of MI. Male and female C57BL6/J mice were fed either a high-fat (60 kJ %) or a low-fat (10 kJ %) diet. Experimental myocardial infarction was induced after 16 weeks of feeding. Left ventricular function was studied by echocardiography. Hematopoietic progenitors and peripheral leukocytes were analysed by flow cytometry. Male obese mice exhibited notably higher body weight, significantly increased myelopoiesis in the spleen and higher leukocyte counts in peripheral blood than their female counterparts. Survival over 56 days after myocardial infarction was significantly impaired in obese compared to lean mice (58% vs. 87%). In obese mice, we found significantly elevated myocardial infarction-induced myelopoiesis in the spleen and higher granulocyte, monocyte and pro-inflammatory macrophage numbers in the myocardium. Moreover, RNA-sequencing and immunohistology revealed enhanced triggering receptor expressed on myeloid cells 1 (TREM1) expression in obese compared to lean mice on day 5 after myocardial infarction. Blockade of TREM1 led to significantly better preservation of systolic function in obese mice. After myocardial infarction, obese mice of both sexes showed enhanced myelopoiesis and impaired survival compared to lean mice. TREM1 blockade might be a promising therapeutic strategy for preserving systolic function in obese patients with myocardial infarction.
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4. Delayed intracardiac remote ischemic preconditioning reduces infarct size in remote myocardium of pigs.
4. 延迟性心内远程缺血预适应减小猪远程心肌梗死面积PMID:日期:2026-08-31Cardioprotection induced by repetitive ischemia/reperfusion (I/R) is not confined to the ischemic region but may extend to distant myocardial territories, a phenomenon termed intracardiac remote ischemic preconditioning (icRIPC). The present study aimed to evaluate the delayed effects of icRIPC on infarct size (IS), left ventricular (LV) function (LVF), and myocardial gene and protein expression. icRIPC was induced in 13 pigs by 3 cycles of 10 min ischemia/10 min reperfusion of the left anterior descending coronary artery (LAD) (conditioning) territory, followed 24 h later by reperfused acute myocardial infarction (AMI) of the left circumflex artery (LCx) (infarcted) territory, induced by 90-min percutaneous balloon occlusion of the mid LCx followed by reperfusion (group icRIPC-AMI). Thirteen additional pigs underwent a sham icRIPC procedure followed by reperfused LCx AMI 24 h later and served as controls (group AMI). Five pigs from each group were euthanized at 3 days, and myocardial expression of nine selected genes was quantified by RT-qPCR in the distal LAD and LCx territories. Protein expression of the two significantly upregulated genes was assessed by Western blot. The remaining eight pigs in each group were followed for 1 month. At 3 days after reperfused AMI, superoxide dismutase-2 (SOD2) protein expression was increased in the infarcted LCx territory of the icRIPC-AMI group, whereas inducible nitric oxide synthase (iNOS/NOS2) protein expression was increased in the distal LAD territory. At 1 month, IS was lower in the icRIPC-AMI than in the AMI group (8.4±3.7% vs. 14.1±1.8% of LV mass, p=0.003), whereas global LVF was marginally improved. However, segmental mean contraction velocity of the infarcted lateral wall was higher in the icRIPC-AMI than in the AMI group (14.8±1.6 vs. 13.3±0.9 mm/s, p=0.026). These findings provide potentially mechanistic evidence for delayed icRIPC, characterized by reduced IS, improved regional myocardial function, and territory-specific changes in cardioprotective protein expression, and may represent an experimental correlate of the clinical phenomenon of pre-infarction angina.
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5. NLRX1 emerges as the only observed essential regulator of the mPTP, challenging mPTP inhibition as a valid target of cardioprotection.
5. NLRX1成为唯一被观察到的mPTP必需调节因子，对mPTP抑制作为心脏保护有效靶点提出了挑战PMID:日期:2026-08-19The mitochondrial permeability transition pore (mPTP) opening is a phenomenon in which the inner mitochondrial membrane abruptly becomes permeable when matrix calcium reaches a critical threshold. Despite 5 decades of intensive research, no protein has been universally accepted as essential for mPTP opening, limiting mechanistic understanding and raising questions about the validity of mPTP-targeted strategies to mitigate cardiac ischemia-reperfusion (I/R) injury. Here, we discuss convergent findings from two independent laboratories identifying the innate immune receptor NLRX1 as an unexpected, essential requirement for mPTP activity. NLRX1 is the only NOD-like receptor (NLR) that is targeted to the mitochondrion. NLRX1 deficiency abolishes (1) calcium-induced mPTP opening, (2) cyclosporine A sensitivity of the pore, and (3) mitochondrial calcium release following cardiac I/R. To test whether loss of mPTP function aligns with loss of NLRX1 across evolution, we performed forward and reciprocal bioinformatic (Blastp) searches and found that species reported to lack an mPTP (e.g., Artemia franciscana and Drosophila melanogaster) also lack NLRX1, further supporting a mandatory role for NLRX1 in mPTP occurrence. Notably, NLRX1-deficient hearts can exhibit increased, rather than decreased, I/R injury at specific ischemia durations. This mirrors reports that deletion of established mPTP regulators (e.g., Ppif) may also worsen injury under defined conditions, consistent with context-dependent, potentially protective roles for transient mPTP activity (e.g., mitochondrial calcium release, PI3K/Akt signaling). In summary, we propose that NLRX1 is the only currently identified protein that is strictly required for mPTP opening, and that indiscriminate inhibition of the mPTP is unlikely to represent a universally effective cardioprotective strategy against I/R injury.
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6. Metabolic dependency of malonate protection against cardiac ischemia-reperfusion injury.
6. 丙二酸对心脏缺血再灌注损伤保护的代谢依赖性PMID:日期:2026-08-17Malonate, an inhibitor of mitochondrial succinate dehydrogenase (SDH), protects against ischemia-reperfusion injury (IRI) when given at early reperfusion, making it a promising therapeutic agent for acute myocardial infarct (AMI) and stroke patients. Prior to clinical studies, it is essential to identify potential translational roadblocks. One such barrier is the metabolic signature of the heart. Here, we explored whether and how the metabolic signature of the heart drive cardiac IRI and modulate malonate protection. Langendorff-perfused mouse hearts were subjected to 30 min ischemia (I) followed by 90 min reperfusion (R), with or without 5mM disodium malonate administered during the first 5 min reperfusion. Cardiac IRI and malonate protection were examined under four metabolic conditions increasing in metabolic complexity: glucose-only (G), glucose + glutamine (GG), GG + fatty acid (F), F + insulin (Ins). Metabolomic profiling and survival kinases were evaluated at end-ischemia and at 7 min of reperfusion ± malonate. Additional experiments examined the effects of glucose, lactate, and low pH on malonate efficacy. IRI (% infarct size) increased with metabolic complexity: 32 ± 11% (G), 38 ± 11%(GG), 52 ± 14% (F), and 68 ± 10% (Ins). Malonate reduced IS% in the G (-27%), GG (-45%) and F (-23%) groups, but not in the Ins group (-12%, not significant). Malonate increased the glycolytic activator and protectant fructose-1/2,6-bisphosphate, mitochondrially bound hexokinase 1 and ATP across all metabolic conditions, confirming measurements showing cellular malonate uptake in all metabolic conditions. Loss of protection correlated with elevated pre-ischemic glycogen levels, end-ischemic lactate levels and delayed ischemic contracture, both indicative of prolonged glycolysis during ischemia due to glycogen loading, and increased glycolytic intermediates during early reperfusion hallmarks of cardiac glucose loading. Indeed, protection was restored in the insulin group when glucose was withheld prior to ischemia. With glucose present before ischemia, elevated lactate and lower pH were observed at onset reperfusion. Further experiments revealed that lower pH-not elevated lactate-at reperfusion was responsible for the loss of malonate protection. Disodium malonate (120 mg/kg) was also unable to reduce infarct size in an in vivo rat model of cardiac IRI employing similar insulin levels as used in the Langendorff-perfused mouse heart model. While malonate offers robust protection against cardiac IRI across various metabolic environments, its efficacy is compromised under conditions of high ischemic glycogen breakdown, which leads to severe acidosis at the onset of reperfusion that was associated with the loss of malonate protection.
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7. TGF-β signalling drives chemotaxis of human induced pluripotent stem cell-derived cardiomyocytes in response to MI stimulus.
7. TGF-β信号驱动人诱导多能干细胞源性心肌细胞对MI刺激的趋化反应PMID:日期:2026-08-12Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) hold significant promise for cardiac regeneration therapies. However, the efficacy of such treatments depends on the ability of transplanted cells to migrate and integrate into the damaged myocardium, a process that remains poorly understood. In this study, we investigated the migratory behaviour of hiPSC-CMs using homogenised rat MI tissue to simulate myocardial infarction (MI) in vitro. Transwell migration assays demonstrated a concentration-dependent chemotactic response, with hiPSC-CM migration increasing up to threefold towards MI tissue homogenate. Wound-healing assays further confirmed enhanced migration under MI-mimetic conditions. Bulk RNA sequencing revealed activation of the TGF-β signalling pathway as a key regulator of this response. Inhibition of TGF-β signalling, both pharmacologically and through antibody neutralisation, significantly reduced hiPSC-CM migration. These findings uncover a previously underappreciated chemotactic capability of hiPSC-CMs and identify TGF-β signalling as a central mediator, offering new mechanistic insights and potential therapeutic targets to improve the integration and efficacy of hiPSC-CM-based cardiac regeneration strategies.
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8. Fast skeletal myosin binding protein-C expression exacerbates dysfunction in heart failure.
PMID:日期:2026-08-05During heart failure (HF), gene and protein expression profiles undergo extensive compensatory and pathological remodeling. We previously observed that fast skeletal myosin binding protein-C (fMyBP-C) is upregulated in diseased mouse hearts. While fMyBP-C shares significant homology with its cardiac paralog, cardiac myosin binding protein-C (cMyBP-C), there are key differences that may affect cardiac function. However, the consequence of cardiac expression of fMyBP-C is unknown. Here, we aim to elucidate the impact of fMyBP-C expression on cardiac function and pathology. To determine the sufficiency of fMyBP-C to cause cardiac dysfunction, we generated cardiac-specific fMyBP-C over-expression mice. These mice were crossed into cMyBP-C null mice to assess the effect of fMyBP-C in the complete absence of cMyBP-C. Finally, fMyBP-C null mice underwent transverse aortic constriction (TAC) to define the requirement of fMyBP-C in HF. We confirmed the upregulation of fMyBP-C in several models of cardiac disease, including lineage tracing models. Low levels of fMyBP-C caused mild cardiac remodeling and sarcomere dysfunction. Exclusive expression of fMyBP-C in a HF model exacerbated cardiac pathology. Furthermore, reduction of fMyBP-C expression by shRNA in HF improved cardiac function. Following pressure overload, fMyBP-C null mice demonstrated greater resistance to cardiac decompensation. Mechanistically, our data suggest the differential regulation of the myosin super-relaxed state by cMyBP-C and fMyBP-C plays a contributing role. These findings suggest the elevated expression of fMyBP-C in diseased hearts is a pathological response. Targeted therapies to prevent upregulation of fMyBP-C may prove beneficial in the treatment of HF.
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9. P38α deficiency alleviates myocardial ischemia/reperfusion injury by stabilizing c‑Myc to inhibit ferroptosis.
9. P38α缺失通过稳定c-Myc抑制铁死亡从而减轻心肌缺血/再灌注损伤PMID:日期:2026-08-04Myocardial ischemia/reperfusion (I/R) injury constitutes a major clinical challenge in ischemic heart disease, and ferroptosis has been recognized as a core driver of cardiomyocyte death during reperfusion. However, the upstream regulatory network governing myocardial ferroptosis remains incompletely defined. The mitogen-activated protein kinase 14 (p38α, MAPK14) is a stress-activated kinase critically involved in cardiac pathophysiology, yet its role in I/R-induced ferroptosis remains unclear. Here, we report that p38α deficiency attenuates ferroptosis and protects against myocardial I/R injury by stabilizing c-Myc. Phosphorylated p38α (p-p38α) was significantly elevated in mouse hearts after I/R and in cardiomyocytes following oxygen-glucose deprivation/reperfusion (OGD/R). Cardiomyocyte-specific p38α knockout markedly reduced ferroptosis, myocardial infarct size, and cardiac dysfunction. Mechanistically, p-p38α interacts with c-Myc under I/R stress via key residues Arg291, Arg300, and Lys304 of c-Myc and promotes the recruitment of the E3 ubiquitin ligase STUB1, thereby enhancing ubiquitination at Lys51 (K51) of c-Myc and its proteasomal degradation. Loss of p38α stabilizes c-Myc protein and reverses this process. Furthermore, c-Myc acts as a transcriptional repressor of NCOA4, a core mediator of ferroptosis. I/R-induced downregulation of c-Myc relieves NCOA4 suppression, triggering iron overload, lipid peroxidation, and ferroptosis. Overexpression of c-Myc or inhibition of STUB1 or NCOA4 abolished the pro-ferroptotic effect of I/R. Pretreatment with the p38α inhibitor VX-745 recapitulated the cardioprotective effects by restoring the p38α/c-Myc/NCOA4 axis in vivo. Collectively, our findings identify the p38α/c-Myc/NCOA4 signaling axis as a regulatory cascade governing myocardial I/R-induced ferroptosis. These findings nominate the p38α/c-Myc/NCOA4 axis as a potential therapeutic target in myocardial I/R injury.
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10. MiR-145-5p modulates collagen production and fibroblast behaviour after cardiac injury partially via COL5A1.
PMID:日期:2026-08-03In contrast to humans, zebrafish hearts after cryoinjury undergo transient fibrotic scarring that subsequently resolves and renews with functional cardiomyocytes. To understand the molecular mechanisms underlying cardiac scarring and fibrotic resolution in zebrafish, we investigated cardiac transcriptomic responses in zebrafish at 14 days post-cryoinjury. Principal component analyses revealed distinct transcriptome clusters corresponding to healthy and injured hearts, highlighting significant changes during cardiac regeneration. Gene set enrichment analyses indicated that extracellular matrix organization and inflammatory response pathways were activated in cryoinjured hearts, while mitochondrial organization and oxidative phosphorylation pathways were downregulated. Notably, miR-145-5p was downregulated and col5a1 upregulated in the cryoinjured hearts, contrasting with the expression patterns of miR-145-5p and COL5α1 in the left ventricles of ischemic cardiomyopathy patients. Prediction of miRNA-mRNA interaction and a dual luciferase assay identified COL5A1 as a target of miR-145-5p. Inhibition of miR-145-5p in human cardiac fibroblasts increased COL5A1 and α-SMA, decreased COL1A, and stimulated fibroblast differentiation, proliferation, and migration. Conversely, overexpression of miR-145-5p led to the opposite effects. Downregulation of COL5A1 suppressed fibroblast proliferation and migration, which could be rescued by inhibition of miR-145-5p. Moreover, downregulation of col5a1 attenuated cardiac fibrotic scar resolution in zebrafish. Interestingly, downregulation of COL5A1 or inhibition of miR-145-5p diminished the expression of integrin subunits ITGβ3 and ITGβ5. Furthermore, inhibition of miR-145-5p potentiated the suppression of TGF-β/SMAD signalling and the enhancement of fibroblast proliferation mediated by inhibiting integrin αvβ3 and αvβ5 with cilengitide. Collectively, miR-145-5p modulates collagen production and fibroblast behaviour partially via targeting COL5A1 and through integrin-mediated pathways.