bioRxiv Science⌕ Search

bioRxiv · 10.64898/2025.12.23.696268

Isoflavone treatment attenuates cardiovascular-kidney-metabolic (CKM) syndrome symptoms in an experimental model of ovariectomized rats.

Abstract

Cardiovascular-kidney-metabolic (CKM) syndrome represents an integrated spectrum of obesity, type 2 diabetes mellitus, cardiovascular disease, and chronic kidney disease, driven by shared metabolic, inflammatory, and fibrotic mechanisms. Menopause-related estrogen deficiency exacerbates these disturbances, increasing susceptibility to metabolic syndrome and renal injury. This study investigated whether dietary supplementation with soy isoflavones attenuates obesity-associated kidney injury in ovariectomized rats exposed to a high-fat, high-caloric diet. Female Wistar rats underwent bilateral ovariectomy and were assigned to control diet, hipercaloric diet (DH), or DH supplemented with isoflavones (DH+ISO). Metabolic, biochemical, oxidative stress, histopathological, and inflammatory parameters were evaluated over 120 days. The DH diet induced weight gain, hypertension, dyslipidemia, hyperglycemia, impaired renal function, increased oxidative stress, and tubulointerstitial injury, consistent with a CKM phenotype. Isoflavone supplementation did not prevent diet-induced weight gain but attenuated systolic blood pressure elevation and improved lipid and glycemic profiles. Renal function was partially preserved in DH+ISO rats, as evidenced by lower plasma creatinine levels, improved creatinine clearance, reduced urea levels, and decreased urinary peroxide excretion compared with DH animals. Histopathological analysis revealed persistent tubular injury in both DH groups, although inflammatory and oxidative markers were attenuated in isoflavone-treated rats. Immunohistochemistry demonstrated reduced renal IL-6 expression in the DH+ISO group, accompanied by trends toward decreased macrophage infiltration and IL-1{beta} expression. Collectively, these findings indicate that soy isoflavones mitigate metabolic, inflammatory, and oxidative pathways implicated in obesity-related kidney injury in a postmenopausal experimental model. Isoflavone supplementation may represent a complementary therapeutic strategy for attenuating CKM-related renal damage associated with modern diets and estrogen deficiency.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Lima, T. d. S., Pessoa, E. d. A., Duarte-Neto, A. N., Borges, C. S., Convento, M. B., Castino, B., Oliveira, A. S., Santos, A. A., Carbonel, A., Dezoti, C., Vattimo, M. d. F., Borges, F. T.. 2025-12-25. Isoflavone treatment attenuates cardiovascular-kidney-metabolic (CKM) syndrome symptoms in an experimental model of ovariectomized rats.. https://doi.org/10.64898/2025.12.23.696268

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Autophagic flux is increased in peripheral blood mononuclear cells in atherosclerotic vascular disease and associates inversely with adverse cardiovascular events

Background: Autophagy is a homeostatic pathway supporting stress adaptation and is dysregulated in atherosclerosis. Its potential as a biomarker or therapeutic target in atherosclerotic vascular disease (ASVD) remains incompletely defined. We measured autophagic flux in peripheral blood mononuclear cells (PBMCs) from patients with peripheral arterial disease (PAD) or carotid stenosis (CS), compared with healthy controls, and explored clinical outcome associations. Methods: Ninety-four patients with PAD or CS and 19 healthy controls were studied. Autophagic flux was quantified from fresh blood using a validated ex vivo chloroquine inhibition ELISA measuring LC3BII accumulation. Major adverse cardiovascular events (MACE) and major adverse limb events (MALE) were ascertained over a median follow up of 828 days. Results: The ASVD cohort comprised claudication (n = 16), chronic limb threatening ischemia (CLTI; n = 49), and CS (n = 29). Autophagic flux was higher in ASVD than controls (mean 281.4 vs. 182.3 ng LC3BII/mg protein/h; p < 0.0001) and remained independently associated after multivariable adjustment. Within CLTI, concurrent infection was associated with lower flux (p = 0.001), approaching control levels (p = 0.327). In CLTI, higher flux quartiles were associated with lower MACE risk, most strongly for quartile 3 (hazard ratio 0.07 vs. quartile 1, 95% CI 0.01 to 0.50; p = 0.009). Conclusion: Autophagic flux is elevated in PBMCs from ASVD patients, independent of age and sex. Attenuated flux in CLTI with concurrent infection may indicate autophagic exhaustion in advanced disease. The association between higher flux and lower MACE in CLTI suggests prognostic utility, warranting evaluation in larger prospective studies.

pathology↗

Quantitative Model of the Ocular Immune Response during Seasonal Allergic Conjunctivitis

Allergic conjunctivitis is an inflammation of the conjunctiva caused by allergen; it is common disorder affecting up to 40% of the population. In this work, we study seasonal allergic conjunctivitis (SAC), also called "hay fever eyes", which is caused by exposure to airborne pollens. We develop a mathematical model quantifying the ocular immune system response to the allergens. First, we present a simplified qualitative description of the immunopathogenesis of SAC. Then, we express each chosen immunopathological mechanism mathematically to construct a system of thirty-one ordinary differential equations. We compare summary statistics of the predicted observable immune signals to experimental measurements and find our model captures key qualitative features of SAC progression. We then compare our predicted time series of histamine concentration to symptom scores and find a strong correlation suggesting the model predicts relevant clinically trends. Next, we calibrate the model through multi-step process. We find the most influential parameters are the production and depletion rates of IL-4, and the production rates of IL-5 and IL-8. These cytokines are targeted in treatments for asthma, atopic dermatitis, and severe eosinophilic associated disorder and suggest potential therapeutic targets for SAC. Our calibrated model mimics most of the summary statistics of the experimentally observable immune signals with discrepancies for IL-5 and IL-13 indicating that additional immunopathological mechanisms could be important.

pathology↗

Dysregulated Platelet GPIb alpha - VWF Signalling in Abdominal Aortic Aneurysm formation and Progression

Background: Platelets are critical drivers of thrombo-inflammatory responses in different cardiovascular diseases. Abdominal aortic aneurysm (AAA) is a progressive, life-threatening vascular disorder mainly characterised by chronic inflammation, extracellular matrix degradation, and the formation of a platelet-rich intraluminal thrombus (ILT). Experimental and clinical evidence identified platelets as main players in AAA pathology as evidenced by elevated platelet activation and procoagulant activity that critically contribute to AAA progression. Methods: The present study investigated the contribution of glycoprotein (GP)Ib alpha, the von Willebrand factor (VWF)-binding subunit of the platelet GPIb-IX-V complex, to AAA initiation and progression in experimental AAA using the ePPE mouse model and in patients. Results: Genetic ablation of platelet GPIb alpha significantly attenuated early aneurysm expansion in experimental AAA, indicating a critical role for GPIb alpha during the initial stages of aneurysm development. This initial effect was compensated at later time points showing no differences in aneurysm progression between groups. Notably, genetic deletion of GPIb alpha induced a constitutively hyperactive platelet phenotype already in naive mice that was further amplified during experimental AAA. This elevated platelet hyperactivity was mainly due to increased GPVI activation of platelets 28 days post-surgery. To assess the clinical relevance, spatial profiles of human ILT specimens from patients with AAA were analysed. In the ILT, we detected a highly compartmentalised distribution of GPIb alpha and VWF with pronounced enrichment within the luminal layer. In parallel, circulating VWF activity as well as platelet surface expression of GPIb alpha were significantly increased in patients with AAA. Conclusion: Collectively, these findings identify a dysregulated GPIb alpha-VWF axis in human AAA pathology, mainly characterised by enhanced platelet GPIb alpha surface expression and increased activity of circulating VWF.

pathology↗