Aging is an inherent phenomenon that is highly important in the pathological development of numerous diseases. Aging is a multidimensional phenomenon characterized by the progressive impairment of various cellular structures and organelle functions. The basis of human organ senescence is cellular senescence. Currently, with the increase in human life expectancy and the increasing proportion of the elderly population, the economic burden of diseases related to aging is becoming increasingly heavy worldwide, and an in-depth study of the mechanism of cellular aging is urgently needed. Aging, a multifactor-driven biological process, is closely related to mitochondrial dysfunction, which is the core pathological basis of a variety of age-related diseases. This article systematically reviews the molecular pathways by which mitochondrial dysfunction drives aging through multidimensional mechanisms such as metabolic reprogramming, epigenetic regulation, telomere damage, autophagy imbalance, and the senescence-associated secretory phenotype. Metabolic reprogramming promotes tumor progression and exacerbates energy metabolism disorders through abnormal activation of the PI3K/Akt/mTOR signaling pathways. The sirtuin family (such as SIRT1 and SIRT3) maintains mitochondrial homeostasis by regulating PGC-1α, FOXO3 and other targets. Telomere shortening directly inhibits mitochondrial biosynthesis through the p53–PGC-1α axis, leading to oxidative stress accumulation and a decline in organ function. The dual roles of autophagy (removing damaged mitochondria or inducing apoptosis) suggests that its homeostasis is essential for delaying aging. The SASP mediates the inflammatory microenvironment through the cGAS‒STING pathway, which is not only a marker of aging but also a driving force of disease progression. Future studies need to integrate multiomics techniques to analyze the interaction network between mitochondria and other organelles, such as the endoplasmic reticulum and lysosomes, and explore precise intervention strategies targeting sirtuins, AMPK and telomerase. Combined therapies targeting metabolic reprogramming or SASP inhibition are expected to provide new ideas for delaying aging and preventing age-related diseases.

Purpose: The effect of the diurnal temperature range (DTR) on human health in diverse geographic areas and the potential confounding factors are not fully understood. Additionally, while a robust association has been reported between temperature and cardiomyopathy (CM), evidence of the impact of DTR is relatively limited. Here, we determined whether an association exists between DTR and CM hospitalisations in vulnerable populations. Methods: CM admission data (2016– 2021) were collected from seven tertiary hospitals in Henan.We used a GAM combined with a distributed lag non-linear model (DLNM) to investigate the delayed effects of DTR on daily hospitalisations for CM.Stratified analysis was performed in subgroups according to sex, age, and season. Attributable fractions (AF) and attributable numbers (AN) were employed to illustrate the disease burden and investigate the association between temperature and DTR. Results: Overall, 5,757 CM cases were identified. DTR and CM admissions exhibited a non-linear correlation. High DTR (P95: 15.5 °C) and low DTR (P05: 3 °C) increased CM admission risk, with low DTR having a stronger effect. Males and warm seasons were significantly more susceptible to DTR, and low DTR affected youth and adults more than older adults. AF and AN of low DTR on CM admissions were 51% and 2,936, respectively. Conclusion: Our results revealed a significant association between DTR and CM hospitalisations, providing valuable insights for the development targeted prevention and control measures.

Cancer has become a focal point of concern owing to its escalating incidence and mortality rates. However, traditional treatment modalities are encumbered by inherent constraints, posing ongoing challenges in achieving definitive cancer eradication. Mitochondria, crucial for cellular growth and physiological homeostasis, manifest distinctive structural and metabolic alterations within cancerous cells compared to their normal counterparts. Targeting aberrant mitochondrial metabolism in tumor cells has emerged as a promising therapeutic strategy, capitalizing on the precision, efficacy, and minimal adverse effects associated with targeted therapeutic approaches. However, due to the complexity of tumor cells, the specific mechanism underlying the role of mitochondria in tumor development and new anti-tumor drugs targeting mitochondrial metabolism still need to be further studied. This review focuses on studies that target mitochondrial DNA, oxidative phosphorylation, mitochondrial energy metabolism, and amino acid metabolism in tumor cells, elucidating the methods involved in targeting mitochondrial metabolism and underscoring the significance of future studies in developing therapies targeting mitochondrial metabolism for cancer treatment.

Neointimal hyperplasia results from irregular vascular smooth muscle cell (VSMC) proliferation and migration. Lycorine hydrochloride (LH), known for its cardioprotective properties, was investigated for its impact on neointimal hyperplasia and underlying mechanisms. In a murine model of left common carotid artery ligation (CAL)-induced neointimal hyperplasia, LH was administered intraperitoneally for 28 days. Further studies investigated LH's impact on MOVAS cells phenotype switching activated by platelet-derived growth factor-BB (PDGF-BB). LH significantly inhibited neointimal hyperplasia in vivo and decreased PDGF-BB-stimulated MOVAS cell proliferation, migration, inflammation and phenotypic transformation in vitro. Mechanistically, LH inhibited PDGF-BB-induced phosphorylation of mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated kinase (Erk1/2), c-Jun terminal kinase (c-Jun), and p38 MAP kinase (p38). Specific inhibitors (PD98059, SP600125, SB203580) diminished PDGF-BB-mediated MOVAS cell phenotypic switching, the potential mechanism involves binding to Erk1 to repress Erk1/2 activation. Therefore, LH suppressed PDGF-BB-mediated VSMCs phenotypic switching and attenuated vascular neointimal hyperplasia at least in part by targeting Ekr1 to regulate the MAPK cascade, indicating its potential as a prevention for restenosis.

We report a case of subacute myocardial infarction thrombus aspiration using extension catheters. The presence of refractory thrombus was observed in all patients during coronary angiography, and favorable outcomes were achieved through the use of an extended catheter for thrombus extraction. In cases involving subacute or refractory thrombus, the efficacy of traditional thrombus aspiration catheters may be limited, necessitating the use of an extension catheter for effective thrombus removal.