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Fibrotic diseases cause annually more than 800,000 deaths worldwide, where of the majority accounts for cardiovascular fibrosis, which is characterized by endothelial dysfunction, myocardial stiffening and reduced dispensability. MicroRNAs (miRs), small noncoding RNAs, play critical roles in cardiovascular dysfunction and related disorders. Intriguingly, there is a critical link among miR-122, cardiovascular fibrosis, sirtuin 6 (SIRT6) and angiotensin-converting enzyme 2 (ACE2), which was recently identified as a coreceptor for SARS-CoV2 and a negative regulator of the rennin-angiotensin system. MiR-122 overexpression appears to exacerbate the angiotensin II-mediated loss of autophagy and increased inflammation, apoptosis, extracellular matrix deposition, cardiovascular fibrosis and dysfunction by modulating the SIRT6-Elabela-ACE2, LGR4-β-catenin, TGFβ-CTGF and PTEN-PI3K-Akt signaling pathways. More importantly, the inhibition of miR-122 has proautophagic, antioxidant, anti-inflammatory, anti-apoptotic and antifibrotic effects. Clinical and experimental studies clearly demonstrate that miR-122 functions as a crucial hallmark of fibrogenesis, cardiovascular injury and dysfunction. Additionally, the miR-122 level is related to the severity of hypertension, atherosclerosis, atrial fibrillation, acute myocardial infarction and heart failure, and miR-122 expression is a risk factor for these diseases. The miR-122 level has emerged as an early-warning biomarker cardiovascular fibrosis, and targeting miR-122 is a novel therapeutic approach against progression of cardiovascular dysfunction. Therefore, an increased understanding of the cardiovascular roles of miR-122 will help the development of effective interventions. This review summarizes the biogenesis of miR-122; regulatory effects and underlying mechanisms of miR-122 on cardiovascular fibrosis and related diseases; and its function as a potential specific biomarker for cardiovascular dysfunction.

Polycystic ovary syndrome (PCOS) is a common endocrine disorder that significantly increases cardiovascular disease (CVD) risk in women. While insulin resistance and dyslipidemia are established contributors, growing evidence highlights mitochondrial dysfunction and chronic low-grade inflammation as central drivers of cardiovascular pathology in PCOS. This narrative review synthesizes current evidence on how mitochondrial dysfunction and inflammation interact to promote cardiovascular complications in women with PCOS while identifying potential therapeutic targets and areas requiring further investigation. A comprehensive review of clinical and experimental studies was conducted using PubMed, Scopus, and Web of Science databases. Relevant literature exploring mitochondrial alterations, oxidative stress, inflammatory cytokines, and endothelial function in PCOS, with emphasis on cardiovascular outcomes, was critically evaluated and summarized. Women with PCOS exhibit altered mitochondrial dynamics, reduced ATP production, and elevated reactive oxygen species (ROS), which collectively impair vascular function. These mitochondrial abnormalities compromise oocyte quality and endometrial receptivity and activate proinflammatory signaling pathways, including the NLRP3 inflammasome, contributing to endothelial dysfunction and atherogenesis, and increased long-term cardiovascular risk, particularly in women with prior pregnancy complications. Elevated levels of cytokines including TNF- , IL-6, and CRP further exacerbate cardiovascular risk. This bidirectional relationship between mitochondrial dysfunction and inflammation establishes a vicious cycle underlying cardiovascular deterioration in PCOS. Mitochondrial dysfunction and inflammation are interdependent mechanisms that contribute substantially to cardiovascular risk in women with PCOS. Targeting mitochondrial dysfunction and systemic inflammation presents a promising therapeutic strategy for reducing cardiovascular morbidity in PCOS. Future research should emphasize phenotype-specific interventions, biomarker discovery, and translational trials to improve long-term reproductive and cardiovascular outcomes.

High serum level of palmitic acid(PA) is implicated in pathogenesis of cardiovascular diseases. PA serves as the substrate for protein palmitoylation. However, it is still unknown whether palmitoylation is involved in PA‐induced cardiovascular dysfunction. Here, in clinical cohort studies of 1040 patients with coronary heart disease, high level of PA is associated with risk of major adverse cardiovascular events (MACE) and death. In ApoE−/−mice, 10 mg/kg−1 PA treatment induces blood pressure elevation, cardiac contractile dysfunction, endothelial dysfunction and atherosclerotic plaqueformation. In endothelial cells, inhibition of palmitoylation bypalmitoyl‐transferase inhibitor 2‐BP eliminates PA‐induced endothelial injury, whereas promotion of palmitoylation by depalmitoylase inhibitor ML349 exacerbates the harmful effect of PA. Palmitoyl‐proteomics analysis identifies pyruvate kinase isozyme type M2 (PKM2) as the palmitoylated protein responsible for PA‐induced endothelial injury, and Cys31 as the predominant palmitoylated site. PKM2‐C31S mutants (cysteine replaced by serine) prevents PA‐induced endothelial injury. Endothelial‐specific AAV‐C31S PKM2endo ameliorates cardiovascular dysfunction caused by PA in ApoE−/− mice. Mechanistically, PKM2‐C31 palmitoylation impairs PKM2 tetramerization to inhibit its pyruvate kinase activity and endothelial glycolysis. Finally, zDHHC13 is identified as the palmitoyl acyltransferase of PKM2. In conclusion, these findings suggest that PKM2‐C31 palmitoylation contributes to PA‐induced endothelial injury and cardiovascular dysfunction. Clinical cohort studies indicate that high serum level of palmitic acid (PA) is associated with risk of cardiovascular events and death. The detrimental effect of PA is attributed to palmitoylation of pyruvate kinase isozyme type M2 (PKM2) at C31 in vascular endothelial cells. PKM2‐C31 palmitoylation impairs PKM2 tetramerization and inhibits endothelial glycolysis, finally resulting to endothelial cell injury and facilitating the development of cardiovascular diseases.

Purpose of Review To evaluate the effectiveness of rehabilitation therapies for managing symptoms of sleep and autonomic dysfunction (cardiovascular, gastrointestinal, urinary and sexual) in Parkinson’s disease (PD). The narrative review focuses on recent data drawn from clinical trials, particularly randomized controlled trials, to assess these therapies and the overall quality of the evidence. Recent Findings Resistance training and aerobic exercises can improve sleep quality in PD. Resistance and aerobic exercises, along with abdominal binders, may help alleviate orthostatic hypotension, though the quality of evidence is not high. Interventions such as expiratory muscle strength training, sensorimotor training, and video-assisted swallowing therapy are beneficial for dysphagia. Pelvic floor muscle training combined with behavioral therapy can potentially mitigate urgency and urge incontinence. Summary Many rehab-based strategies though promising lack sufficient evidence for implementation into clinical practice. The current evidence supports their role in addressing sleep disturbances, orthostatic hypotension and dysphagia. However, the evidence for their effectiveness in treating gastroparesis, constipation, and urinary and sexual dysfunction remains limited.

New Findings What is the topic of this review? Thermal extremes disproportionately affect populations with cardiovascular conditions. Preterm birth, across all gestational age ranges below 37 weeks, has been identified as a non‐modifiable risk factor for cardiovascular disease. The hypothesis is presented that individuals born preterm are at an increased risk of cardiovascular morbidity and mortality during thermal extremes. What advances does it highlight? Cardiovascular stress tests performed in preterm‐born populations, from infancy through adulthood, highlight a progression of cardiovascular dysfunction accelerating through adolescence and adulthood. This dysfunction has many similarities with populations known to be at risk in thermal extremes. Preterm‐born individuals are a uniquely vulnerable population. Preterm exposure to the extrauterine environment and the (mal)adaptations that occur during the transitional period can result in alterations to their macro‐ and micro‐physiological state. The physiological adaptations that increase survival in the short term may place those born preterm on a trajectory of lifelong dysfunction and later‐life decompensation. Cardiovascular compensation in children and adolescents, which masks this trajectory of dysfunction, is overcome under stress, such that the functional cardiovascular capacity is reduced and recovery impaired following physiological stress. This has implications for their response to thermal stress. As the Anthropocene introduces greater changes in our environment, thermal extremes will impact vulnerable populations as yet unidentified in the climate change context. Here, we present the hypothesis that individuals born preterm are a vulnerable population at an increased risk of cardiovascular morbidity and mortality during thermal extremes.

Spinal cord injury (SCI) leads to severe impairment in cardiovascular control, commonly manifested as a rapid, uncontrolled rise in blood pressure triggered by peripheral stimuli—a condition called autonomic dysreflexia. The objective was to demonstrate the translational potential of noninvasive transcutaneous stimulation (TCS) in mitigating autonomic dysreflexia following SCI, using pre-clinical evidence and a clinical case report. In rats with SCI, we show that TCS not only prevents the instigation of autonomic dysreflexia, but also mitigates its severity when delivered during an already-triggered episode. Furthermore, when TCS was delivered as a multisession therapy for 6 weeks post-SCI, the severity of autonomic dysreflexia was significantly reduced when tested in the absence of concurrent TCS. This treatment effect persisted for at least 1 week after the end of therapy. More importantly, we demonstrate the clinical applicability of TCS in treatment of autonomic dysreflexia in an individual with cervical, motor-complete, chronic SCI. We anticipate that TCS will offer significant therapeutic advantages, such as obviating the need for surgery resulting in reduced risk and medical expenses. Furthermore, this study provides a framework for testing the potential of TCS in improving recovery of other autonomic functions such lower urinary tract, bowel, and sexual dysfunction following SCI.

Global longitudinal strain (GLS) is an echocardiographic measure to detect chemotherapy-related cardiovascular dysfunction. However, its limited availability and the needed expertise may restrict its generalization. Artificial intelligence (AI)-based GLS might overcome these challenges. Our aims are to explore the agreements between AI-based GLS and conventional GLS, and to assess whether the agreements were influenced by expertise levels, cardiac remodeling and cardiovascular diseases/risks. Echocardiographic images in the apical four-chamber view of left ventricle were retrospectively analyzed based on AI-based GLS in patients treated with chemotherapy, and correlation between AI-based GLS (Caas Qardia, Pie Medical Imaging) and conventional GLS (Vivid E9/VividE95, GE Healthcare) were assessed. The agreement between unexperienced physicians (“GLS beginner”) and experienced echocardiographer were also assessed. Among 94 patients (mean age 69 ± 12 years, 73% female), mean left ventricular ejection fraction was 64 ± 6%, 14% of patients had left ventricular hypertrophy, and 21% had left atrial enlargement. Mean GLS was − 15.9 ± 3.4% and − 19.0 ± 3.7% for the AI and conventional method, respectively. There was a moderate correlation between these methods (rho = 0.74; p < 0.01), and bias was − 3.1% (95% limits of agreement: -8.1 to 2.0). The reproducibility between GLS beginner and an experienced echocardiographer was numerically better in the AI method than the conventional method (inter-observer agreement = 0.82 vs. 0.68). The agreements were consistent across abnormal cardiac structure and function categories (p-for-interaction > 0.10). In patients treated with chemotherapy. AI-based GLS was moderately correlated with conventional GLS and provided a numerically better reproducibility compared with conventional GLS, regardless of different levels of expertise.

Background The maternal cardiovascular system undergoes a profound transformation during pregnancy. Disordered cardiovascular adaptation is associated with pre-eclampsia and fetal growth restriction; however, these complications remain challenging to predict and manage. Computational modelling presents an opportunity to study the maternal circulation with unprecedented flexibility. We conducted a scoping review to assess the potential utility of computational models for studying maternal cardiovascular adaptation to pregnancy and providing insights into disease. We aimed to identify research gaps and barriers to translating this emerging field into clinical practice. Methods Medline, Embase, and Web of Science Core Collection were searched from 01/01/2013 to 01/09/2025, for articles related to computational haemodynamic models of pregnancy. English-language studies describing models of the maternal circulation in human pregnancy were identified. Information on system modelled, study design, participant or clinical specimen details, and key findings were extracted from original research studies and presented in a narrative synthesis. Results Of 662 citations, 37 met inclusion criteria, comprising 28 original research studies, two conference abstracts, and seven reviews. Amongst the original research studies, 27 were basic experimental papers and one was a retrospective cohort study. Nine experimental articles incorporated data from pregnant participants or clinical specimens into personalised models, with sample sizes between one and 21. Four of these included participants or specimens affected by hypertensive disorders of pregnancy or fetal growth restriction. The retrospective cohort study employed haemodynamic modelling to investigate blood loss in 480 patients with abnormally invasive placentas. Modelling approaches described included those simulating the entire maternal circulation, maternal cardiac remodelling, maternal renal autoregulation, the maternal pelvic circulation in isolation, uterine vascular adaptation, spiral artery remodelling, and blood flows within the placental intervillous space. Conclusions Computational modelling could represent a powerful tool to advance understanding of maternal cardiovascular adaptation to pregnancy and guide future approaches to risk stratification, diagnosis, and management of pregnancy complications. Realising this promise will require cardiovascular models to be parameterised with scalable metrics, validated in large pregnancy cohorts, developed alongside robust computational processing pipelines, and integrated into existing clinical workflows. Protocol registration The review protocol was registered prospectively with the Open Science Framework (osf.io/v3968).

Advanced glycation end products (AGEs) are a group of proteins and lipids becoming glycated and oxidized after persistent contact with reducing sugars or short-chain aldehydes with amino group and/or high degree of oxidative stress. The accumulation of AGEs in the body is a natural process that occurs with senescence, when the turnover rate of proteins is reduced. However, increased circulating AGEs have been described to arise at early lifetime and are associated with adverse outcome and survival, in particular in settings of cardiovascular diseases. AGEs contribute to the development of cardiac dysfunction by two major mechanisms: cross-linking of proteins or binding to their cell surface receptor. Recently, growing evidence shows that high-molecular weight AGEs (HMW-AGEs) might be as important as the characterized low-molecular weight AGEs (LMW-AGEs). Here, we point out the targets of AGEs in the heart and the mechanisms that lead to heart failure with focus on the difference between LMW-AGEs and the less characterized HMW-AGEs. As such, this review is a compilation of relevant papers in the form of a useful resource tool for researchers who want to further investigate the role of HMW-AGEs on cardiac disorders and need a solid base to start on this specific topic.

Cardiac troponin serum concentration is the primary marker used for the diagnosis of acute coronary syndrome. Moreover, the measurement of cardiac troponin concentration is important for risk stratification in patients with pulmonary embolism. The cardiac troponin level is also a general marker of myocardial damage, regardless of etiology. The purpose of this study is to conduct a literature review and present the most important information regarding the current state of knowledge on the cardiac troponin serum concentration in patients with chronic cardiovascular disease (CVD), as well as on the relationships between cardiac troponin serum concentration and features of subclinical cardiovascular dysfunction. According to research conducted to date, patients with CVDs, such as chronic coronary syndrome, chronic lower extremities’ ischemia, and cerebrovascular disease, are characterized by higher cardiac troponin concentrations than people without a CVD. Moreover, the literature data indicate that the concentration of cardiac troponin is correlated with markers of subclinical dysfunction of the cardiovascular system, such as the intima–media thickness, pulse wave velocity, ankle–brachial index, coronary artery calcium index (the Agatston score), and flow-mediated dilation. However, further research is needed in various patient subpopulations and in different clinical contexts.