Vascular remodeling is a common pathological hallmark of many cardiovascular diseases. Vascular smooth muscle cells (VSMCs) are the predominant cell type lining the tunica media and play a crucial role in maintaining aortic morphology, integrity, contraction and elasticity. Their abnormal proliferation, migration, apoptosis and other activities are tightly associated with a spectrum of structural and functional alterations in blood vessels. Emerging evidence suggests that mitochondria, the energy center of VSMCs, participate in vascular remodeling through multiple mechanisms. For example, peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α)-mediated mitochondrial biogenesis prevents VSMCs from proliferation and senescence. The imbalance between mitochondrial fusion and fission controls the abnormal proliferation, migration and phenotypic transformation of VSMCs. Guanosine triphosphate-hydrolyzing enzymes, including mitofusin 1 (MFN1), mitofusin 2 (MFN2), optic atrophy protein 1 (OPA1) and dynamin-related protein 1 (DRP1), are crucial for mitochondrial fusion and fission. In addition, abnormal mitophagy accelerates the senescence and apoptosis of VSMCs. PINK/Parkin and NIX/BINP3 pathways alleviate vascular remodeling by awakening mitophagy in VSMCs. Mitochondrial DNA (mtDNA) damage destroys the respiratory chain of VSMCs, resulting in excessive ROS production and decreased ATP levels, which are related to the proliferation, migration and apoptosis of VSMCs. Thus, maintaining mitochondrial homeostasis in VSMCs is a possible way to relieve pathologic vascular remodeling. This review aims to provide an overview of the role of mitochondria homeostasis in VSMCs during vascular remodeling and potential mitochondria-targeted therapies.

Antimicrobial use (AMU) is the major driver of antimicrobial resistance (AMR) among bacteria in dairy herds. There have been numerous studies on AMU and AMR in dairy cows; however, studies on AMU and AMR in dairy calves are limited. A comprehensive overview of the current state of knowledge of AMU and AMR among pathogens in dairy calves is important for the development of scientifically supported and applicable measures to curb antimicrobial use and the increasing risk of AMR. Therefore, we performed a systematic review of research on AMU and AMR in dairy calves. A total of 75 publications were included, of which 19 studies reported AMU data for dairy calves and 68 described AMR profiles of the four most prevalent bacteria that are associated with calf diarrhea and calf pneumonia. Large variation in AMU was found among herds across different regions. There seems to be a positive association between exposure to antimicrobials and occurrence of resistance. Most AMU was accounted for by treatment of diseases, while a small proportion of AMU was prophylactic. AMU was more common in treating calf diarrhea than in treating pneumonia, and the resistance rates in bacteria associated with diarrhea were higher than those in pathogens related to pneumonia. Organic farms used significantly fewer antimicrobials to treat calf disease; however, the antimicrobial resistance rates of bacteria associated with calf diarrhea and pneumonia on both types of farms were comparable. Feeding waste or pasteurized milk was associated with a higher risk of AMR in pathogens. Altogether, this review summarizes AMU and AMR data for dairy calves and suggests areas for future research, providing evidence for the design of antimicrobial use stewardship programs in dairy calf farming.

Vascular inflammation triggers the development of thoracic aortic dissection (TAD). Zinc deficiency could dampen tissue inflammation. However, the role of zinc as a nutritional intervention in the progression of TAD remains elusive. In this study, we employed a classical β-aminopropionitrile monofumarate (BAPN)-induced TAD model in mice treated with low zinc and observed that the TAD progression was greatly ameliorated under low zinc conditions. Our results showed that low zinc could significantly improve aortic dissection and rupture (BAPN + low zinc vs. BAPN, 36% vs. 100%) and reduce mortality (BAPN + low zinc vs. BAPN, 22% vs. 57%). Mechanically, low zinc attenuated the infiltration of macrophages and inhibited the expression of inflammatory cytokines, suppressed the phenotype switch of vascular smooth muscle cells from contractile to synthetic types, and eventually alleviated the development of TAD. In conclusion, this study suggested that low zinc may serve as a potential nutritional intervention approach for TAD prevention.