Heart failure (HF) in the setting of diabetes represents a distinct cardiometabolic phenotype characterized by profound disturbances in myocardial glucose metabolism, mitochondrial function, and energetic efficiency. Growing evidence indicates that sirtuins, a family of nicotinamide adenine dinucleotide (NAD+)-dependent deacylases, play a central role in coordinating glucose utilization, oxidative metabolism, and stress responses in the heart. Findings from genetically modified animal models and cardiomyocyte studies demonstrate that sirtuin impairment, often driven by NAD+ depletion and redox imbalance, further suppresses metabolic activity and promotes metabolic inflexibility, whereas restoration of NAD+ availability or sirtuin activity improves mitochondrial efficiency and metabolic coordination. Human studies, including analyses of myocardial tissue and circulating biomarkers, provide supportive but largely associative evidence, highlighting a substantial translational gap. In this review, we synthesize experimental and clinical data linking sirtuin signaling to the metabolic remodeling observed in diabetic HF, with particular emphasis on glycolysis-oxidation uncoupling, pyruvate dehydrogenase regulation, and mitochondrial dysfunction. We critically discuss context-dependent effects, apparent contradictions, and current limitations of the field, emphasizing differences between diabetic and non-diabetic HF, as well as phenotype- and stage-specific considerations. Finally, we explore therapeutic implications and outstanding questions, positioning the NAD+-sirtuin axis as a unifying mechanistic framework that links systemic metabolic disease to cardiac energetic failure and underscores the potential for metabolism-informed, precision strategies in diabetic HF.

Sirtuins are an evolutionarily conserved family of nicotinamide adenine dinucleotide (NAD+)-dependent enzymes that regulate aging, cellular stress responses, and metabolic homeostasis. In mammals, seven isoforms (SIRT1-SIRT7) differ in subcellular localization, substrate specificity, and enzymatic activity, allowing them to control genomic stability, mitochondrial function, redox balance, inflammation, apoptosis, autophagy, and cell proliferation. Increasing evidence links sirtuin dysregulation to age-related chronic diseases, particularly cardiovascular disease (CVD). This review provides an integrated overview of the structure, enzymatic functions, localization, and biological specialization of mammalian sirtuins, with an emphasis on their roles in physiological aging and cardiovascular homeostasis. We discuss the involvement of individual sirtuins in major cardiovascular pathologies, including metabolic cardiomyopathy, myocardial ischemia-reperfusion injury (IRI), cardiac hypertrophy, fibrosis, heart failure, atherosclerosis, coronary artery disease, and hypertension. Particular focus is placed on SIRT1, SIRT3, and SIRT6, which emerge as key regulators of endothelial integrity, mitochondrial quality control, oxidative stress, inflammatory signaling, and myocardial remodeling. We also highlight the context-dependent and sometimes dual effects of other sirtuin isoforms in CVD. Finally, we summarize current therapeutic strategies targeting sirtuins, including activators, NAD+-boosting approaches, and selective inhibitors, and discuss the main challenges for future clinical translation in cardiovascular medicine, including precision, isoform-specific intervention design strategies, and long-term clinical implementation.

ObjectiveThis narrative review aims to examine potential associations between migraine and retinal disorders, with particular attention to retinal migraine, age-related macular degeneration (AMD), retinal vascular occlusions, and photophobia.BackgroundThe role of retinal pathways in migraine pathophysiology remains poorly understood. As a component of the central nervous system, the retina provides a unique and accessible window into neuronal structure and function. Emerging observations suggest that structural and functional retinal changes may occur in individuals with migraine; however, their relevance and consistency across studies remain uncertain.ResultsVisual phenomena are characteristic of migraine aura, yet the extent to which migraine affects retinal structure and function is still unclear. Retinal migraine, while suggestive of a direct retinal involvement, is rare and insufficiently characterized to support mechanistic conclusions. Epidemiological data indicate that individuals with migraine may have an increased risk of neovascular AMD, raising the possibility of shared pathogenic pathways. In addition, photophobia, retinal artery occlusion, and alterations in retinal nerve fiber layer thickness have been reported more frequently in migraine patients than in controls, although causality has not been established. Mechanisms implicated in AMD, including microvascular dysfunction, impaired DNA damage response, disrupted autophagy, and mitochondrial dysregulation, have also been proposed in migraine, but evidence remains limited.ConclusionMigraine has been linked to several retinal conditions, with AMD showing the most consistent association. While overlapping biological processes are suggested, further studies are needed to clarify their significance and determine whether retinal alterations contribute to migraine pathophysiology or represent secondary phenomena.

Cellular senescence, a state where cells permanently exit the cycle but remain metabolically active, plays a role in cardiovascular diseases (CVD), including heart failure (HF). Senescent cells accumulate in aging and stressed heart tissue, releasing pro-inflammatory cytokines, chemokines, and enzymes that affect endothelial cells. This ongoing inflammation exacerbates cardiac damage, induces endothelial dysfunction, and triggers secondary senescence across various cardiac cell types. Senescent cardiomyocytes contribute to reduced systolic function by causing mitochondrial damage, impaired contractility, and metabolic dysfunction, leading to lower cardiac output and symptoms such as fatigue and exercise intolerance in HF patients. Additionally, inflammation from senescent endothelial cells and loss of microvasculature impair coronary blood flow and oxygen delivery, worsening symptoms such as shortness of breath, angina-like discomfort, and fluid retention by disrupting cardiac energy metabolism and increasing filling pressures. A key factor linking cellular senescence with HF is sirtuin 1 (SIRT1), a histone deacetylase with antioxidant activity. SIRT1 acts as a hormetic regulator in the heart, being beneficial within a narrow range but potentially harmful when overstimulated. As drugs targeting senescence are emerging to treat CVD, it is important to evaluate how SIRT1 may influence the connection between senescence and HF to improve anti-senescent therapies. In this narrative/perspective review, we explore the molecular mechanisms underlying senescence in HF development and how SIRT1 might modulate these processes for therapeutic benefit.

Background: Iron deficiency (ID) is a prevalent condition in patients with cardiovascular diseases, irrespective of anemia, associated with adverse outcomes. Its incidence and prognostic value in acute coronary syndromes (ACS) are yet to be established. Current literature on the matter is scarce, and further research is necessary to confirm a clear link between ID and possible adverse outcome prediction in this group. Aims: This study aimed to evaluate the incidence and prognostic value of ID in ACS patients, and associations between iron parameters and patients' characteristics, comorbidities, hospitalization length, laboratory results, electrocardiographic, echocardiographic assessment, and invasive coronary angiography results. Methods: We conducted an observational prospective study enrolling 214 consecutive patients after ACS. Adverse events were defined as all-cause death or non-elective rehospitalization due to cardiovascular causes. Results: ID patients constituted 46.7% of the studied cohort. ID was associated with higher NT-proBNP on admission (p = 0.03). Higher TSAT was independently associated with lower peak troponin levels (β = -0.03, standardized β = -0.15, p = 0.03). Ferritin < 100 ng/mL was paradoxically associated with shorter in-hospital stay (p = 0.03). In multivariable analysis, ID was an independent predictor of the composite endpoint (HR 1.94 [95% CI: 1.02-3.67], p = 0.04); however, no significant differences in event-free survival have been identified between ID and non-ID groups. Conclusions: ID is a common condition in ACS patients, associated with higher values of biomarkers reflecting cardiac damage, and may constitute an important predictor of adverse events after discharge. Further, larger, preferably multicenter studies are required to establish the exact association between ID and mortality among ACS patients treated with percutaneous coronary intervention.

Migraine may signal early signs of aging-related processes, such as reduced autophagy, increased reactive oxygen and nitrogen species (RONS), and low-grade inflammation in people prone to migraine, without necessarily indicating systemic aging. While migraine is not an age-related condition, brain aging might be accelerated by cellular senescence in neurons and glia, contributing to cognitive decline in migraine patients. Although neurons are postmitotic cells, they can undergo postmitotic cellular senescence, which may contribute to the chronicity of migraine. Oxidative stress is a key factor inducing senescence and also plays a role in migraine development, as the brains of migraine sufferers show an over-reliance on mitochondria that produce an excess of RONS. These RONS can lower the threshold for cortical spreading depression and directly activate trigeminovascular nociceptors through RONS-sensitive ion channels, resulting in calcitonin gene-related peptide-dependent migraine pain. Excessive RONS can also damage DNA, and abnormal repair of single-strand DNA breaks caused by migraine-related brain activity may connect migraine with senescence. Defects in autophagy could activate cellular senescence and stabilize senescence-associated secretory phenotype. Impaired autophagy in microglia might trigger secretory autophagy and the release of brain-derived nuclear factor, which could induce autophagy in neurons to eliminate cellular debris caused by oxidative stress. This sequence of events is possible but has not yet been demonstrated in material from migraine patients and animal models. Cellular senescence may influence migraine through various mechanisms, including oxidative stress, cortical spreading depression, abnormal DNA damage responses, and impaired autophagy. Currently, there is no direct evidence linking cellular senescence to migraine, but it is unclear whether such research has been conducted to date, and we have argued that these studies are warranted.

Increasing epidemiological and experimental evidence suggests that age-related macular degeneration (AMD) and cardiovascular disease (CVD) share multiple pathogenic mechanisms. Among these, oxidative stress has emerged as one of the most plausible links connecting retinal degeneration and cardiovascular pathology. Excessive production of reactive oxygen and nitrogen species, combined with declining antioxidant defenses, contributes to lipid peroxidation, mitochondrial dysfunction, chronic inflammation, complement activation, cellular senescence, and impaired cellular stress responses in both the retina and the vascular system. Notably, drusen (AMD) and atherosclerotic plaques (CVD) share several molecular constituents. Therefore, AMD and CVD may represent tissue-specific manifestations of broader age-related disturbances in redox homeostasis and inflammatory regulation. Nevertheless, the coexistence of AMD and CVD is incomplete, suggesting that genetic susceptibility, tissue-specific responses to oxidative stress, biological aging, and mechanisms of cellular resilience influence disease expression. In this review, we summarize current evidence linking AMD and CVD, examine oxidative stress-driven molecular pathways common to both disorders, discuss emerging biomarkers and therapeutic targets, and highlight important unresolved questions regarding disease heterogeneity and causal relationships. A better understanding of the shared mechanisms underlying AMD and CVD may facilitate the development of integrated preventive strategies, improved risk stratification, and more personalized therapeutic approaches for age-related diseases.

BACKGROUND:Patients with osteoporosis (OP) have an increased 10-year cardiovascular death risk. Low bone mineral density (BMD) observed in OP may be associated with arrhythmic presentation of cardiovascular diseases. AIMS:We assessed arrhythmia occurrence in females with osteoporosis. METHODS:One hundred three postmenopausal females, consulted by an endocrinologist, were divided into 2 groups according to BMD (assessed by dual-energy X-ray absorptiometry), expressed as T-score (T-sc; OP ≤-2.5, control >-2.5), taken from the femoral neck (T-sc Neck), the entire total hip (T-sc TH), and/or the spine (T-sc L2-L4, L1-L4). The occurrence of arrhythmia was evaluated using 24-hour Holter electrocardiography monitoring (HM). Major osteoporotic and total hip fracture risks (MOFR and THFR, respectively) were assessed by the FRAX scale. RESULTS:Arrhythmic burden correlated with BMD: correlations were observed between the number of ventricular ectopic beats (VEB) in HM and the T-sc Neck (r = -0.20; P = 0.04), T-sc TH (r = -0.22; P = 0.03) as well as between the number of supraventricular ectopic beats (SVEB) in HM and the T-sc Neck (r = -0.21; P = 0.03), and T-sc TH (r = -0.23; P = 0.02). Multivariable analysis (linear regression model) showed age and T-sc TH as independently related with ectopy: age (b = 0.07; 95% CI, 0.01-0.13; P = 0.03) and T-sc TH (b = -0.58; 95% CI, -1.07 to -0.08; P = 0.02) were predictors for VEB. Ectopic beats count was also positively correlated with osteoporotic fracture risk: VEB with THFR (r = 0.206; P = 0.04), and SVEB with MOFR (r = 0.21; P = 0.04). CONCLUSIONS:Postmenopausal women diagnosed with osteoporosis are likely to have higher risk of ventricular and supraventricular arrhythmias than women without osteoporosis. Moreover, we documented that the presence of cardiac arrhythmia increases with the risk of osteoporotic fractures.

BACKGROUND:Studies of animal and human aortic tissue samples showed that sirtuins may protect against aortic aneurysm (AA). However, to date, no studies have assessed plasma or serum sirtuin levels in humans. Therefore, the aim of this study was to evaluate associations between plasma sirtuin 1 (SIRT1) and sirtuin 2 (SIRT2) levels and the presence of ascending AA. METHODS:Plasma SIRT1 and SIRT2 levels were assessed in patients with and without ascending AA using an enzyme-linked immunosorbent assay. RESULTS:The study included 32 patients with ascending AA (median age: 67 years) and 37 controls without AA (median age: 68 years). Plasma SIRT1 and SIRT2 levels did not differ between groups (p > 0.05). However, slightly higher sirtuin levels were observed in patients with ascending AA than in controls, particularly for SIRT1 in the subgroups of patients without coronary artery disease, atrial fibrillation, and chronic obstructive pulmonary disease (COPD). Among patients with ascending AA, higher SIRT2 levels were noted for those without COPD vs. those with COPD (p = 0.04). CONCLUSIONS:The study showed no significant differences in SIRT1 and SIRT2 levels between patients with and without ascending AA. However, there was a trend towards higher SIRT1 levels in patients with AA, especially in those without comorbidities.

It is critical to sustain the diversity of the microbiota to maintain host homeostasis and health. Growing evidence indicates that changes in gut microbial biodiversity may be associated with the development of several pathologies, including type 2 diabetes mellitus (T2DM). Metformin is still the first-line drug for treatment of T2DM unless there are contra-indications. The drug primarily inhibits hepatic gluconeogenesis and increases the sensitivity of target cells (hepatocytes, adipocytes and myocytes) to insulin; however, increasing evidence suggests that it may also influence the gut. As T2DM patients exhibit gut dysbiosis, the intestinal microbiome has gained interest as a key target for metabolic diseases. Interestingly, changes in the gut microbiome were also observed in T2DM patients treated with metformin compared to those who were not. Therefore, the aim of this review is to present the current state of knowledge regarding the association of the gut microbiome with the antihyperglycemic effect of metformin. Numerous studies indicate that the reduction in glucose concentration observed in T2DM patients treated with metformin is due in part to changes in the biodiversity of the gut microbiota. These changes contribute to improved intestinal barrier integrity, increased production of short-chain fatty acids (SCFAs), regulation of bile acid metabolism, and enhanced glucose absorption. Therefore, in addition to the well-recognized reduction of gluconeogenesis, metformin also appears to exert its glucose-lowering effect by influencing gut microbiome biodiversity. However, we are only beginning to understand how metformin acts on specific microorganisms in the intestine, and further research is needed to understand its role in regulating glucose metabolism, including the impact of this remarkable drug on specific microorganisms in the gut.

INTRODUCTION: Anemia and vitamin D deficiency are thought to significantly impact the clinical course in patients diagnosed with heart failure (HF). Both conditions are prevalent within the general population, and their incidence increases among HF patients. We investigated the prognostic value of anemia and 25-hydroxyvitamin D [25(OH)D] deficiency in patients with heart failure with reduced and mildly reduced ejection fraction. MATERIAL AND METHODS: The study was prospective and was conducted on 87 patients diagnosed with HF. The patients were assigned to 2 groups depending on the left ventricular ejection fraction (LVEF): HFrEF if LVEF ≤ 40% (n = 49) and HFmrEF if LVEF = 41–49% (n = 38). Hemoglobin levels and 25-hydroxyvitamin D concentration were measured. Survival analysis was performed after 1 and 10 years of follow-up. RESULTS: The prevalence of vitamin D deficiency among patients classified as HFmrEF and HFrEF was 66% and 49%, respectively, demonstrating a higher occurrence than anemia, which was observed in 24% and 31% of participants. In univariate analysis, 25(OH)D concentration < 20 ng/mL was found to be a significant risk of death during the 10-year follow-up period in the entire study group (OR: 95% CI: 2.64; 1.1–6.32, p = 0.029). There was no statistically significant effect of anemia on the prognosis in patients with heart failure. Univariate and multivariate analysis showed that NYHA class > II was a significant prognostic factor for 10-year mortality in the study population (OR: 95% CI: 2.52; 1.002–6.33, p = 0.0495). CONCLUSIONS: Vitamin D deficiency and NYHA class > II showed prognostic value as a predictor of 10-year mortality in the study population. A high prevalence of vitamin D deficiency and anemia, regardless of left ventricular ejection fraction, was confirmed.

Atrial fibrillation (AF) is the most common cardiac arrhythmia. Yet, its treatment has serious challenges and is unsuccessful in a considerable fraction of patients. One reason may be a limited understanding of the molecular mechanisms underlying AF. Recent studies suggest that oxidative stress is involved in AF pathogenesis. Enhanced oxidative stress is largely determined by disrupted mitochondrial homeostasis, as cardiomyocytes heavily rely on mitochondrial energy production and calcium transfer between mitochondria and the sarcoplasmic reticulum. Atrial fibrillation involves metabolic, structural, and electrical remodeling, all of which are influenced by mitochondrial mechanisms. Mitochondrial homeostasis is controlled by mitochondrial quality control (mtQC), which is a multi-pathway mechanism to maintain integrity and functionality of mitochondria. Impaired mtQC may result in disturbed mitochondria-related calcium handling, decreased energy production, mitochondria-related inflammation and fibrosis, and impaired mitophagy. Sirtuins (SIRTs) are a family of seven members of histone deacetylases which have antioxidant properties, and three of them are localized to mitochondria. Therefore, at least some SIRTs may ameliorate enhanced oxidative stress related to damaged mitochondria. SIRTs have shown potential to improve AF outcomes in studies on AF patients and animal models. Therefore, SIRTs may have potential to ameliorate AF by decreasing oxidative stress and restoring mitochondrial homeostasis disrupted in AF. In this narrative review, we provide information on how mitochondrial dysfunctions, expressed as a disturbance in mtQC, contribute to AF through oxidative stress, calcium handling abnormalities, energy deficiency, inflammation and fibrosis, and genetic changes. In addition, we present the protective potential of sirtuins in AF.

Heart failure (HF) has become an emerging problem, especially in regions where life expectancy is increasing. Despite its prevalence, the mechanisms behind HF development are not well understood, which is reflected in the lack of curative therapies. Mitochondria, autophagy, and sirtuins form a crucial triad involved in HF pathogenesis, interconnected by oxidative stress. Identifying a common pathway involving these three components could be valuable in developing new treatment strategies. Since HF is the end result of several cardiovascular diseases, this review highlights the main HF precursors and explores the roles of mitochondrial quality control (mtQC), autophagy, and sirtuins in HF development. Dysfunctional mitochondria may play a key role by enhancing oxidative stress and influencing autophagy and sirtuins, both of which possess antioxidant properties. The dual nature of autophagy—its pro-life and pro-death roles—may contribute to different outcomes in HF related to oxidative stress. As mtQC, autophagy, and sirtuins may interact, we present data on their mutual dependencies in HF. However, the specificity of these interactions remains unclear and needs further investigation, which could help identify new therapeutic targets. In conclusion, the interplay between mtQC, autophagy, and sirtuins may be crucial in HF pathogenesis and could be leveraged in developing HF treatments.

Acute coronary syndromes (ACS) are a leading cause of death and impairment in the adult population. Precise identification and modification of risk factors is crucial for a favorable clinical outcome. In this review, we aim to provide a comprehensive overview of the significance of iron deficiency (ID) in patients with ACS, particularly myocardial infarction (MI). The paper evaluates the impact of ID on the prognosis of ACS patients, highlighting its potential influence on myocardial healing, regeneration and cardiovascular events during the follow-up period. The findings suggest that iron deficiency may have a negative impact on the prognosis of patients with MI, resulting in worse quality of life, physical capacity and higher rehospitalization rates in comparison to patients with normal iron status. Iron supplementation in patients with MI could be beneficial and may have an effect on myocardial healing and left ventricular remodeling.

Wstęp. Choroba wieńcowa jest jednym z najczęściej występujących problemów kardiologicznych zarówno w Polsce, jak i na świecie. W przypadku wielonaczyniowej choroby wieńcowej (MVD) kwestia dalszego postępowania i leczenia jest jeszcze bardziej skomplikowana. Nieinwazyjne metody obrazowania są powszechnie stosowane w diagnozowaniu choroby wieńcowej. Celem niniejszej pracy była analiza porównawcza wyników tomografii komputerowej tętnic wieńcowych (CCTA) i koronarografii w odniesieniu do zmiennych demograficznych i klinicznych u pacjentów z MVD. Materiał i metody. Badanie przeprowadzono u 106 pacjentów z MVD hospitalizowanych w Klinice Kardiologii Centralnego Szpitala Klinicznego w Łodzi. Analizie poddano dostępne wyniki CCTA i koronarografii, porównując wyniki pod kątem istotności zwężeń w tętnicach wieńcowych w obu badaniach. Przeprowadzono również charakterystykę demograficzną oraz kliniczną analizowanej grupy pacjentów. Wyniki. Znaczną większość pacjentów stanowili mężczyźni (n = 69,8%). Średnia wieku pacjentów wynosiła 69,42 ± 8,28 lat. Czynniki ryzyka choroby wieńcowej były rozpowszechnione w dużym stopniu w badanej populacji. Całościowa zgodność w ocenie istotności zwężeń w tętnicach wieńcowych w badaniu CCTA w porównaniu z koronarografią wynosiła 73% (κ = 0,47). Największa zgodność w ocenie dotyczyła pnia lewej tętnicy wieńcowej 78% (κ = 0,5), a najmniejsza —gałęzi okalającej 69% (κ = 0,34). Wnioski. U pacjentów z MVD występuje umiarkowana zgodność pomiędzy opisem istotności zwężeń w tętnicach wieńcowych w badaniu CCTA w porównaniu do koronarografii. Tomografia komputerowa tętnic wieńcowych, jako metoda nieinwazyjna, jest jednym z narzędzi w początkowej diagnostyce przy podejrzeniu choroby wieńcowej. Czynniki ryzyka choroby wieńcowej są szeroko rozpowszechnione i stanowią istotny problem w analizowanej populacji pacjentów.

Background Previous studies explored multifactorial interactions and sirtuin expression in the aortic cells of laboratory rodents and humans. Human studies were limited due to the availability of biological material exclusively in the advanced stage of the disease. The role of sirtuins in aortic pathology has not been explained extensively therefore the aim of the study was to assess the plasma concentrations of human sirtuin 1 (SIRT1) and human sirtuin 2 (SIRT2) in patients with ascending aortic dissection and ascending aortic aneurysm. Material and methods The study group included 43 adults (34 males and 9 females) aged 44–92 years with ascending aortic dissection ( n = 10) or with ascending aortic aneurysm ( n = 33). The SIRT1 and SIRT2 plasma concentrations in patients’ blood samples were determined, and the differences between groups were observed ( p = 0.02 for SIRT1, p = 0.04 for SIRT2). Results Levels of both SIRT1 and SIRT2 were lower in patients with ascending aortic dissection (SIRT1: median = 6.5 ng/mL; SIRT2: median = 5.7 ng/mL) than in patients with ascending aortic aneurysm (SIRT1: median = 9.2 ng/mL; SIRT2: median = 7.8 ng/mL). The SIRT1 and SIRT2 cut-off levels differentiating both groups of patients were 6.7 ng/mL and 3.2 ng/mL, respectively. Conclusions The patients with ascending aortic dissection had lower plasma concentrations of SIRT1 and SIRT2 than the patients with ascending aortic aneurysm. Calculated cut-off values for both enzymes may be helpful in laboratory differentiation of ascending aortic dissection from ascending aortic aneurysm.

Objective: Percutaneous transluminal angioplasty (PTA) is the recommended revascularization strategy in patients with renal artery stenosis (RAS) caused by fibromuscular dysplasia (FMD), limiting stenting to complications management. However this recommendation is based on cases reports and small series. The main aim of the study was to retrospectively analyze immediate and long-term results of renal stenting and PTA in FMD patients. The second aim was to evaluate the results of stenting as support of renal artery aneurysm (RAA) closure. Design and method: The study group consisted of 58 patients percutaneously treated due to significant RAS (70 arteries) and 9 patients (10 RAAs) with a history of stent implantation before aneurysm embolization, derived from 343 ARCADIA-POL registry patients. PTA was performed as initial treatment in 61 arteries (PTA-group), whereas primary stenting was done in 9 arteries (STENT-group). Stent-related complications(SRC) were defined as: in-stent restenosis (>50%) or occlusion (ISR/O); stent fracture; stent underexpansion (SU) or migration. Results: In PTA-group, the first restenosis rate was 50.8%. Subsequently, 22 arteries underwent a second procedure: re-PTA(12 arteries) or stent implantation(10 arteries) . The incidence of recurrent restenosis after re-PTA was 41.7%. In the 10 arteries initially treated with PTA that underwent stenting for restenosis, complications occurred in 7 of them (70%), including 2 SUs and 5 ISR/Os . In STENT-group, SU occurred in one case (11.1%) and in-stent restenosis in 33.3% (3 of 9 stents). In combined analysis, SRC occurred following 11/19 stenting procedures (57.9%) including 3 periprocedural (SUs) and 8 late complications (ISR/Os). Finally, despite several subsequent revascularization attempts, 4 of 19 (21%) stented arteries were totally occluded and one remained significantly stenosed at follow-up imaging (Figure). In contrast to FMD-RAS procedures, there was only one intraprocedural complication (partial stent migration) and no late SRC in RAA patients. Conclusions: Renal artery stenting in FMD provides modest benefit in terms of restenosis prevention but poses high risk of immediate and late complications, including stent occlusion. Our study supports recommendations limiting stenting to the management of complications. In contrast, renal artery stenting in FMD RAA closure is associated with favorable long-term outcomes.