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The lymphatic system is a unidirectional network in which lymph fluid flows centripetally along a series of lymphatic channels and eventually into the veins, so the lymphatic system can also be considered an auxiliary part of the venous system and an important part of the cardiovascular system. The lymphatic system, which regulates interstitial fluid balance, lipid absorption, and immune monitoring, and its imbalance can lead to a variety of diseases. The pulmonary lymphatic system plays a very important role in many lung diseases, involving maintaining fluid balance, antigen presentation, etc., in addition, it will affect the survival of the transplant after lung transplantation. This article focuses on pulmonary lymphatic vessels and their role in lung disease.

Given the information overload of scientific literature, there is an increasing need for computable biomedical knowledge buried in free text. This study aimed to develop a novel approach to extracting and measuring uncertain biomedical knowledge from scientific statements.

Background: Currently, pathophysiological mechanisms of post‐acute sequelae of coronavirus disease‐19‐cardiovascular syndrome (PASC‐CVS) remain unknown. Methods and results: Patients with PASC‐CVS exhibited significantly higher circulating levels of severe acute respiratory syndrome‐coronavirus‐2 spike protein S1 than the non‐PASC‐CVS patients and healthy controls. Moreover, individuals with high plasma spike protein S1 concentrations exhibited elevated heart rates and normalized low frequency, suggesting cardiac β‐adrenergic receptor (β‐AR) hyperactivity. Microscale thermophoresis (MST) assay revealed that the spike protein bound to β1‐ and β2‐AR, but not to D1‐dopamine receptor. These interactions were blocked by β1‐ and β2‐AR blockers. Molecular docking and MST assay of β‐AR mutants revealed that the spike protein interacted with the extracellular loop 2 of both β‐ARs. In cardiomyocytes, spike protein dose‐dependently increased the cyclic adenosine monophosphate production with or without epinephrine, indicating its allosteric effects on β‐ARs. Conclusion: Severe acute respiratory syndrome‐coronavirus‐2 spike proteins act as an allosteric β‐AR agonist, leading to cardiac β‐AR hyperactivity, thus contributing to PASC‐CVS. [ABSTRACT FROM AUTHOR]

The morbidity and mortality of cardiovascular diseases are increasing globally. Pathological cardiac remodeling plays an important role in the development of cardiovascular diseases. More and more investigations focus on the alterations of cardiac metabolism in pathological cardiac remodeling. Cardiac substrate metabolism is severely impaired during cardiac hypertrophy and heart failure, a shift from fatty acid metabolism toglucose metabolism, resulting in aggravated cardiac dysfunction. This review analyzes the relationship amongthe metabolism of different substrates in pathological cardiac remodeling. Based on these metabolic changes, wesummarize the pharmacological agents, and raise new drug development strategies from the perspective of metabolic regulation, leading to an improved prognosis and treatment of patients with cardiac remodeling diseases.

Context: Carnitine has been associated with cardiac energy metabolism and heart failure, but the association between its precursors--trimethyllysine (TML) and γ-butyrobetaine (GBB)--and heart failure with preserved ejection fraction (HFpEF) remains unclear. Objective: To evaluate the relationship between TML-related metabolites and HFpEF in an Asian population. Methods: The cross-sectional component of this study examined the association between plasma TML-related metabolites and HFpEF, while a prospective cohort design was applied to examine the association with incident cardiovascular events in HFpEF. Included in the study were 1000 individuals who did not have heart failure (non-HF) and 1413 patients with HFpEF. Liquid chromatography mass spectrometry was used to assess plasma carnitine, GBB, TML and trimethylamine-N-oxide (TMAO) concentrations. Results: Plasma GBB and TML were both elevated in patients with HFpEF. After adjusting for traditional risk factors and renal function, TML, but not GBB, was significantly associated with HFpEF. The odds ratio (OR) for the fourth vs first quartile of TML was 1.57 (95% CI 1.09-2.27; P-trend<.01). The OR for each SD increment of log-TML was 1.26 (95% CI 1.08-1.47). Plasma TMAO (P-interaction=0.024) and estimated glomerular filtration rate (P-interaction=0.024) modified the TML-HFpEF association. The addition of TML improved the diagnostic value under the multivariable model. In the prospective study of patients with HFpEF, higher plasma TML was associated with increased risk of cardiovascular events. Conclusion: Plasma TML concentrations are positively associated with HFpEF, and higher plasma TML indicates increased risk of cardiovascular events. [ABSTRACT FROM AUTHOR]