Cardiovascular & Hematological Agents in Medicinal Chemistry (Formerly Current Medicinal Chemistry - Cardiovascular & Hematological Agents) - Online First
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Adropin and Spexin Peptides Ameloriate Cardiac Inflammation, Matrix Metalloproteinases, and Vascular Response
Authors: Gülsün Memi, Burak Yazgan and Ebru TaştekinAvailable online: 09 May 2025More LessBackgroundChronic renal failure (CRF) triggers chronic systemic inflammation and causes vascular calcification, a prominent contributor to the progression of cardiovascular disease. Adropin and spexin peptides regulate energy balance; also, these peptides trigger anti-inflammatory pathways.
ObjectiveOur present study aimed to clarify the potentially protective impact of spexin and adropin peptides on cardiovascular inflammation in an adenine-induced chronic renal failure model.
MethodsThe CRF model in Sprague-Dawley rats was established by the administration of adenine hemisulfate for ten days. Then, rats were treated with saline or adropin, or/and spexin for four weeks. CRP, CK, and CK-MB levels in serum were measured by autoanalyzer. Aortic contraction-relaxation responses were determined by the organ bath system. H&E, PAS, and Masson's trichrome stainings evaluated histopathological alterations in both aorta and cardiac tissue. Gene expression levels of ILs (IL1β, IL10, IL17A, IL18, IL21, and IL33), MMPs (MMP1, MMP2, MMP3, MMP9, MMP13, and MMP14), NGAL, TGFβ1, TIMP1, and TNFα in cardiac tissue were evaluated by real-time PCR.
ResultsWe found increased CK and CK-MB levels by CRF induction. In addition, IL1β, IL17A, IL18, IL21, MMP1, MMP3, MMP13, and MMP14 increased after CRF progression. While adropin has effects on CK levels, spexin decreases CK-MB levels. Also, adropin and spexin had a nitric oxide-dependent impact on vascular reactivity. Besides, spexin downregulated IL1β, IL10, IL17A, TGFβ1, MMP1, MMP3, MMP9, MMP13, MMP14 and NGAL; however, the adropin peptide had a limited effect.
ConclusionThese results suggest that adropin and spexin have potential preventive roles on vascular damage in CRF progression via modulation of MMPs and inflammatory genes.
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MOTS-c as a Potential Diagnostic-prognostic Biomarker for Myocardial Infarction
Authors: Abdulkadir Çakmak and Burak YazganAvailable online: 09 May 2025More LessBackgroundMyocardial infarction (MI) is a disease characterised by myocardial necrosis due to acute and prolonged ischaemic hypoxia in the coronary arteries. MOTS-c is a mitochondrial-derived peptide that has been reported to have protective effects on cardiac tissue. Although this peptide is thought to be decreased in various diseases and can serve as a potential biomarker, current studies remain limited.
ObjectiveThis study aimed to evaluate how the post-treatment process affects circulating MOTS-c peptide levels in myocardial infarction patients.
MethodsFor this purpose, patients without obstructive coronary lesions on angiography were included in the control group, while those with significant obstructive coronary lesions on angiography were included in the infarction group. Routine biochemistry tests were performed using an autoanalyzer. Besides, serum MOTS-c levels were measured using ELISA.
ResultsOur findings showed CRP, ESR, and troponin I levels to be higher in the MI group compared to the control group. Also, there was no significant change in MOTS-c levels between the control and the MI group, while time-dependent changes (day 0, day 3, and day 30) occurred within the MI group. However, a negative correlation was found between MOTS-c and platelet levels in the MI group at day 0 (r: -0.4417, p =0.0450). Similarly, MOTS-c was found to be negatively correlated with troponin I in the MI group at day 3 (r: -0.4571, p =0.0372).
ConclusionThe negative correlation of MOTS-c level with both platelet and troponin I has shown that this peptide may contribute to the diagnostic and therapeutic evaluation of the MI process along with other parameters.
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Oxidative Stress in Cardiovascular Diseases: Mechanisms and Exploring Advanced Therapies
Authors: Dushyant, Balram, Gurvirender Singh, Nitish Kumar, Smita Narwal and Ashwani K. DhingraAvailable online: 26 February 2025More LessThe recognition of oxidative stress as a factor influencing the development and progression of cardiovascular diseases (CVDs) is growing. By producing such reactive oxygen species (ROS) in diverse areas within cells, including mitochondria and Nicotinamide Adenine Dinucleotide Phosphate Hydrogen (NADPH)-oxidases, they end up causing damage through the oxidation of lipids, proteins, and DNA. ROS indicates the beginning of inflammatory responses and endothelial dysfunction, which are necessary to produce obstructions in blood vessels and decreased blood vessel function. The fact that oxidative stress plays a significant role in CVD development draws more attention to the need for novel therapies that aim to correct redox imbalances. Therefore, natural polyphenols and antioxidants like vitamin C or E have shown their efficacy in lowering levels of ROS and protecting against the damage caused by oxidative stress. Anyone attempting to cure CVDs should focus on improving the safety and efficacy of antioxidant treatments and identifying which patients will benefit from them the most. This paper discusses not only advanced treatments but also the role played by oxidative stress in such CVD as high blood pressure, hypercholesterolemia, and ischemic heart disease.
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Emerging Biomarkers for Assessing Thrombotic Risk in Patients Receiving Direct Oral Anticoagulants (DOACs)
Authors: Ashmi Sabana M. and Alwin Simon M.Available online: 16 December 2024More LessDirect Oral Anticoagulants (DOACs) have transformed the management of thrombotic disorders, offering a more convenient and effective alternative to traditional vitamin K antagonists (VKAs). However, assessing thrombotic risk in patients treated with DOACS remains crucial due to the potential for recurrent events. Current clinical risk scores have limitations in predicting and monitoring venous thromboembolism (VTE) risk in specific DOAC populations. Several emerging biomarkers show promise in assessing thrombotic risk in patients treated with DOACS. Genetic factors like VKORC1 and CYP2C9 variants are well-established determinants of warfarin response, but the genetic landscape for DOAC outcomes appears more complex. Rare variants and polygenic approaches may play a role in personalizing anticoagulation therapy. Elevated factor VIII levels are associated with increased VTE recurrence risk after anticoagulation withdrawal in cancer-associated thrombosis (CAT) patients. In contrast, the circulating tissue factor is not useful for predicting VTE in this setting. Soluble P-selectin has emerged as a good marker of VTE recurrence, and its inclusion in the Vienna CATS risk model improves VTE prediction in cancer patients. While these biomarkers hold promise, larger studies are needed to validate their utility and establish standardized assays. Caution is warranted in patients at high bleeding risk. Integrating clinical factors, genetics, and circulating biomarkers will likely optimize thrombotic risk assessment in patients treated with DOACS. Continued research is crucial to develop personalized anticoagulation strategies to balance thrombosis and bleeding risks.
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