Heart failure is characterized by progressive energetic insufficiency, in which mitochondrial dysfunction and impaired fatty acid oxidation are central features. Normally, the FAO provides most of the cardiac ATP supply, but in HF, this pathway becomes disrupted, leading to the accumulation of lipid intermediates, oxidative stress, and reduced ATP production. Emerging evidence suggests that mitochondrial impairment and FAO disturbances may interact reciprocally, forming a vicious cycle that aggravates energetic failure and structural remodeling. This review summarizes current knowledge on the bidirectional relationship between mitochondrial dysfunction and FAO abnormalities in HF. We integrate findings from experimental models with clinical observations that highlight the translational relevance of this interplay. In addition, we provide an updated overview of therapeutic strategies, including pharmacological modulators such as SGLT2 inhibitors and trimetazidine, as well as traditional Chinese medicine formulas such as Qiliqiangxin and Qishen granules, which have shown preliminary benefits in clinical studies. Although the proposed vicious cycle remains a working hypothesis requiring further validation, understanding this interplay may help identify novel biomarkers, stratify patients by metabolic phenotype, and guide precision therapies for HF.

Heart failure (HF) has a severe impact on public health development due to high morbidity and mortality and is associated with imbalances in cardiac immunoregulation. Macrophages, a major cell population involved in cardiac immune response and inflammation, are highly heterogeneous and polarized into M1 and M2 types depending on the microenvironment. M1 macrophage releases inflammatory factors and chemokines to activate the immune response and remove harmful substances, while M2 macrophage releases anti-inflammatory factors to inhibit the overactive immune response and promote tissue repair. M1 and M2 restrict each other to maintain cardiac homeostasis. The dynamic balance of M1 and M2 is closely related to the Traditional Chinese Medicine (TCM) yin-yang theory, and the imbalance of yin and yang will result in a pathological state of the organism. Studies have confirmed that TCM produces positive effects on HF by regulating macrophage polarization. This review describes the critical role of macrophage polarization in inflammation, fibrosis, angiogenesis and electrophysiology in the course of HF, as well as the potential mechanism of TCM regulation of macrophage polarization in preventing and treating HF, thereby providing new ideas for clinical treatment and scientific research design of HF.

Background: Atrial fibrillation (AF) is a common arrhythmia that can result in adverse cardiovascular outcomes but is often difficult to detect. The use of machine learning (ML) algorithms for detecting AF has become increasingly prevalent in recent years. This study aims to systematically evaluate and summarize the overall diagnostic accuracy of the ML algorithms in detecting AF in electrocardiogram (ECG) signals. Methods: The searched databases included PubMed, Web of Science, Embase, and Google Scholar. The selected studies were subjected to a meta-analysis of diagnostic accuracy to synthesize the sensitivity and specificity. Results: A total of 14 studies were included, and the forest plot of the meta-analysis showed that the pooled sensitivity and specificity were 97% (95% confidence interval [CI]: 0.94–0.99) and 97% (95% CI: 0.95–0.99), respectively. Compared to traditional machine learning (TML) algorithms (sensitivity: 91.5%), deep learning (DL) algorithms (sensitivity: 98.1%) showed superior performance. Using multiple datasets and public datasets alone or in combination demonstrated slightly better performance than using a single dataset and proprietary datasets. Conclusions: ML algorithms are effective for detecting AF from ECGs. DL algorithms, particularly those based on convolutional neural networks (CNN), demonstrate superior performance in AF detection compared to TML algorithms. The integration of ML algorithms can help wearable devices diagnose AF earlier.

Diabetic nephropathy (DN), a leading cause of end-stage renal disease, is associated with high morbidity and mortality rates worldwide and the development of new drugs to treat DN is urgently required. Bu-Shen-Huo-Xue (BSHX) decoction is a traditional Chinese herbal formula, made according to traditional Chinese medicine (TCM) theory, and has been used clinically to treat DN. In the present study, we established a high-fat diet/streptozotocin-induced diabetic mouse model and treated the mice with BSHX decoction to verify its therapeutic effects in vivo. Ultraperformance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS) was applied to analyze the chemical composition and active compounds of BSHX decoction. Markers of podocyte epithelial-mesenchymal transition and the Rac1/PAK1/p38MAPK signaling pathway were evaluated to investigate the mechanism underlying function of BSHX decoction. BSHX decoction effectively alleviated diabetic symptoms, according to analysis of the renal function indicators, serum creatinine, blood urea nitrogen, serum uric acid, and urinary albumin excretion rate, as well as renal histopathology and ultrastructural pathology of DN mice. We identified 67 compounds, including 20 likely active compounds, in BSHX decoction. The podocyte markers, nephrin and podocin, were down-regulated, while the mesenchymal markers, α-SMA and FSP-1, were up-regulated in DN mouse kidney; however, the changes in these markers were reversed on treatment with BSHX decoction. GTP-Rac1 was markedly overexpressed in DN mice and its levels were significantly decreased in response to BSHX decoction. Similarly, levels of p-PAK1 and p-p38MAPK which indicate Rac1 activation, were reduced on treatment with BSHX decoction. Together, our data demonstrated that BSHX decoction ameliorated renal function and podocyte epithelial-mesenchymal transition via inhibiting Rac1/PAK1/p38MAPK signaling pathway in high-fat diet/streptozotocin-induced diabetic mice. Further, we generated a quality control standard and numerous potential active compounds from BSHX decoction for DN.

PCSK9, which is closely related to atherosclerosis, is significantly expressed in vascular smooth muscle cells (VSMCs). Moreover, Proprotein Convertase Subtilisin/Kexin type 9 (PCSK9) mediated phenotypic transformation, abnormal proliferation, and migration of VSMCs play key roles in accelerating atherosclerosis. In this study, by utilizing the significant advantages of nano-materials, a biomimetic nanoliposome loading with Evolocumab (Evol), a PCSK9 inhibitor, was designed to alleviate atherosclerosis. In vitro results showed that (Lipo + M)@E NPs up-regulated the levels of α-SMA and Vimentin, while inhibiting the expression of OPN, which finally result in the inhibition of the phenotypic transition, excessive proliferation, and migration of VSMCs. In addition, the long circulation, excellent targeting, and accumulation performance of (Lipo + M)@E NPs significantly decreased the expression of PCSK9 in serum and VSMCs within the plaque of ApoE^−/− mice.