Associação entre diabetes e insuficiência cardíaca: mecanismos, fatores de risco e implicações clínicas DOI Creative Commons

Roger Antônio Morais Queiroz,

Hanna Victoria Marinho Oliveira Garcia,

Geraldo Magela Pereira

et al.

Caderno Pedagógico, Journal Year: 2025, Volume and Issue: 22(1), P. e13212 - e13212

Published: Jan. 10, 2025

Introdução: a revisão investigou relação entre diabetes mellitus (DM) e insuficiência cardíaca congestiva (ICC), evidenciando o impacto negativo do DM nos desfechos clínicos, como mortalidade hospitalizações. Mecanismos fisiopatológicos, resistência à insulina, inflamação crônica remodelamento cardíaco, foram destacados fatores que agravam progressão da ICC. Metodologia: analisados estudos publicados 2013 2023, em inglês, português espanhol, selecionados nas bases PubMed, Scopus, Cochrane Library, LILACS SciELO. A seleção incluiu ensaios clínicos randomizados, revisões sistemáticas observacionais, priorizando aqueles com relevância qualidade abordassem ICC, intervenções terapêuticas clínicos. Resultados :os resultados demonstraram exacerba ICC por mecanismos fibrose miocárdica. Novas terapias, os inibidores cotransportadora de sódio-glicose tipo 2 (SGLT2), eficazes na redução hospitalizações mortalidade, além apresentarem benefícios renais significativos. Desenvolvimento: revisados enfatizaram importância um manejo integrado, equilibrando controle glicêmico farmacológicas, para abordar múltiplos fisiopatológicos. Estratégias multidisciplinares são fundamentais otimizar cuidados desfechos. Conclusão: reforça estratégias personalizadas no pacientes foco uso novas terapias cuidado multidisciplinar. Pesquisas futuras devem explorar populações sub-representadas, idosos frágeis renal avançada.

Association between METS-IR and heart failure: a cross-sectional study DOI Creative Commons
Xiaozhou Su, Chunli Zhao, Xianwei Zhang

et al.

Frontiers in Endocrinology, Journal Year: 2024, Volume and Issue: 15

Published: July 1, 2024

Prior research has indicated the importance of insulin resistance in development heart failure (HF). The metabolic score for (METS-IR), a novel measure assessing resistance, been found to be associated with cardiovascular disease (CVD). Nevertheless, relationship between METS-IR and remains uncertain.

Language: Английский

Citations

11
Interleukin-1β polarization in M1 macrophage mediates myocardial fibrosis in diabetes DOI Creative Commons
Wenli Guo, Chen Yang, Jiawei Zou

et al.

International Immunopharmacology, Journal Year: 2024, Volume and Issue: 131, P. 111858 - 111858

Published: March 15, 2024

Language: Английский

Citations

10
Mitochondrial quality control in diabetic cardiomyopathy: from molecular mechanisms to therapeutic strategies DOI Creative Commons
Chen Cai, Feng Wu, Jing He

et al.

International Journal of Biological Sciences, Journal Year: 2022, Volume and Issue: 18(14), P. 5276 - 5290

Published: Jan. 1, 2022

In diabetic cardiomyopathy (DCM), a major complication, the myocardium is structurally and functionally altered without evidence of coronary artery disease, hypertension or valvular disease.Although numerous anti-diabetic drugs have been applied clinically, specific medicines to prevent DCM progression are unavailable, so prognosis remains poor.Mitochondrial ATP production maintains energetic requirements cardiomyocytes, whereas mitochondrial dysfunction can induce aggravate by promoting oxidative stress, dysregulated calcium homeostasis, metabolic reprogramming, abnormal intracellular signaling apoptosis in cardiomyocytes.In response dysfunction, quality control (MQC) system (including fission, fusion, mitophagy) activated repair damaged mitochondria.Physiological fission fragments network isolate mitochondria.Mitophagy then allows dysfunctional mitochondria be engulfed autophagosomes degraded lysosomes.However, MQC results excessive impaired fusion delayed mitophagy, causing fragmented accumulate this review, we summarize molecular mechanisms discuss how pathological contributes development.We present promising therapeutic approaches improve progression.

Language: Английский

Citations

36
Mitochondrial Dysfunction and Mitophagy in Type 2 Diabetes: Pathophysiology and Therapeutic Targets DOI
Nadezda Apostolova, Teresa Vezza, Jordi Muntané

et al.

Antioxidants and Redox Signaling, Journal Year: 2023, Volume and Issue: 39(4-6), P. 278 - 320

Published: Jan. 15, 2023

Significance: Type 2 diabetes mellitus, which is related to oxidative stress and mitochondrial dysfunction, one of the most prevalent diseases in world. In past decade, alterations autophagy have been shown play a fundamental role development control type diabetes. Further, mitophagy has recognized as key player eliminating dysfunctional mitochondria this disease. Recent Advances: Recently, much progress made understanding molecular events associated with stress, Critical Issues: Despite increasing evidence relationship between their pathophysiolology diabetes, effective therapeutic strategies combat disease through targeting mitochondria, autophagy, are yet be implemented. Future Directions: This review provides wide perspective existing literature concerning complicated interplay mitophagy, dysfunction potential targets based on these mechanisms explored. Antioxid. Redox Signal. 39, 278-320.

Language: Английский

Citations

23
The Contribution of Cardiac Fatty Acid Oxidation to Diabetic Cardiomyopathy Severity DOI Creative Commons
Qutuba G. Karwi,

Qiuyu Sun,

Gary D. Lopaschuk

et al.

Cells, Journal Year: 2021, Volume and Issue: 10(11), P. 3259 - 3259

Published: Nov. 21, 2021

Diabetes is a major risk factor for the development of cardiovascular disease via contributing and/or triggering significant cellular signaling and metabolic structural alterations at level heart whole body. The main cause mortality morbidity in diabetic patients including cardiomyopathy. Therefore, understanding how diabetes increases incidence cardiomyopathy it mediates perturbations cell energy metabolism should help therapeutics to prevent these perturbations. One marked increase cardiac fatty acid oxidation rates domination acids as source heart. This increased reliance on has negative impact function structure through number mechanisms. It also detrimental effect efficiency worsens status diabetes, mainly inhibiting glucose oxidation. Furthermore, accelerated make more vulnerable ischemic injury. In this review, we discuss altered insulin resistance contribution overall ATP production efficiency. influences susceptibility myocardium ischemia/reperfusion injury role changes mediating effects are discussed.

Language: Английский

Citations

37
Current understanding on pathogenesis and effective treatment of glycogen storage disease type Ib with empagliflozin: new insights coming from diabetes for its potential implications in other metabolic disorders DOI Creative Commons
Arianna Maiorana, Francesco Tagliaferri, Carlo Dionisi‐Vici

et al.

Frontiers in Endocrinology, Journal Year: 2023, Volume and Issue: 14

Published: April 21, 2023

Glycogen storage type Ib (GSDIb) is a rare inborn error of metabolism caused by glucose-6-phosphate transporter (G6PT, SLC37A4 ) deficiency. G6PT defect results in excessive accumulation glycogen and fat the liver, kidney, intestinal mucosa into both glycogenolysis gluconeogenesis impairment. Clinical features include hepatomegaly, hypoglycemia, lactic acidemia, hyperuricemia, hyperlipidemia, growth retardation. Long-term complications are liver adenoma, hepatocarcinoma, nephropathy osteoporosis. The hallmark GSDIb neutropenia, with impaired neutrophil function, recurrent infections inflammatory bowel disease. Alongside classical nutritional therapy carbohydrates supplementation immunological granulocyte colony-stimulating factor, emerging role 1,5-anhydroglucitol pathogenesis dysfunction led to repurpose empagliflozin, an inhibitor renal glucose SGLT2: current literature its off-label use patients reports beneficial effects on clinical consequences. Surprisingly, this glucose-lowering drug ameliorated glycemic metabolic control patients. Furthermore, numerous studies from big cohorts 2 diabetes showed efficacy empagliflozin reducing cardiovascular risk, progression kidney disease, NAFLD syndrome. Beneficial have also been described peripheral neuropathy prediabetic rat model. Increasing evidences highlight regulating cellular energy sensors SIRT1/AMPK Akt/mTOR, which leads improvement mitochondrial structure stimulation autophagy, decrease oxidative stress suppression inflammation. Modulation these pathways shift lipids oxidation crucial insulin levels, resistance, glucotoxicity lipotoxicity. For pleiotropic effects, appears be good candidate for repurposing other diseases presenting organ damage, defective autophagy.

Language: Английский

Citations

15
miR-340-5p Mediates Cardiomyocyte Oxidative Stress in Diabetes-Induced Cardiac Dysfunction by Targeting Mcl-1 DOI Creative Commons
Yinghong Zhu, Xuewen Yang, Jing Zhou

et al.

Oxidative Medicine and Cellular Longevity, Journal Year: 2022, Volume and Issue: 2022, P. 1 - 21

Published: Jan. 27, 2022

Diabetic cardiomyopathy (DCM) is initially characterized by early diastolic dysfunction, left ventricular remodeling, hypertrophy, and myocardial fibrosis, it eventually clinical heart failure. MicroRNAs (miRNAs), endogenous small noncoding RNAs, play significant roles in diabetes mellitus (DM). However, still largely unknown about the mechanism that links miRNAs development of DCM. Here, we aimed to elucidate underlying potential role microRNA-340-5p DCM db/db mouse, which a commonly used model type 2 DM diabetic complications lead We first demonstrated miR-340-5p expression was dramatically increased tissues mice cardiomyocytes under conditions. Overexpression exacerbated DCM, reflected extensive fibrosis more serious dysfunction as represented apoptotic cardiomyocytes, elevated ROS production, impaired mitochondrial function. Inhibition tough decoy (TUD) vector beneficial for preventing production apoptosis, thus rescuing cardiomyopathy. identified myeloid cell leukemia 1 (Mcl-1) major target gene showed inhibition Mcl-1 responsible functional loss mitochondria, oxidative stress, cardiomyocyte thereby caused cardiac mice. In conclusion, our results plays crucial can be targeted therapeutic intervention.

Language: Английский

Citations

22
Metformin Collaborates with PINK1/Mfn2 Overexpression to Prevent Cardiac Injury by Improving Mitochondrial Function DOI Creative Commons
Zhuang Ma, Zuheng Liu, Xudong Li

et al.

Biology, Journal Year: 2023, Volume and Issue: 12(4), P. 582 - 582

Published: April 11, 2023

Both mitochondrial quality control and energy metabolism are critical in maintaining the physiological function of cardiomyocytes. When damaged mitochondria fail to be repaired, cardiomyocytes initiate a process referred as mitophagy clear defective mitochondria, studies have shown that PTEN-induced putative kinase 1 (PINK1) plays an important role this process. In addition, previous indicated peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) is transcriptional coactivator promotes metabolism, mitofusin 2 (Mfn2) fusion, which beneficial for Thus, integration strategy involving biogenesis might contribute improved cardiomyocyte function. We studied PINK1 isoproterenol (Iso)-induced injury transverse aortic constriction (TAC)-induced myocardial hypertrophy. Adenovirus vectors were used induce PINK1/Mfn2 protein overexpression. Cardiomyocytes treated with (Iso) expressed high levels low Mfn2, changes time dependent. overexpression promoted mitophagy, attenuated Iso-induced reduction MMP, reduced ROS production apoptotic rate. Cardiac-specific cardiac function, pressure overload-induced hypertrophy fibrosis, facilitated TAC mice. Moreover, metformin treatment dysfunction by inhibiting generation leading increase both ATP membrane potential injury. Our findings indicate combination may help ameliorate improving quality.

Language: Английский

Citations

13
The role of circadian clock-controlled mitochondrial dynamics in diabetic cardiomyopathy DOI Creative Commons

Zhenshuai Jin,

Yanwei Ji, Wating Su

et al.

Frontiers in Immunology, Journal Year: 2023, Volume and Issue: 14

Published: May 5, 2023

Diabetes mellitus is a metabolic disease with high prevalence worldwide, and cardiovascular complications are the leading cause of mortality in patients diabetes. Diabetic cardiomyopathy (DCM), which prone to heart failure preserved ejection fraction, defined as cardiac dysfunction without conventional risk factors such coronary hypertension. Mitochondria centers energy metabolism that very important for maintaining function heart. They highly dynamic response environmental changes through mitochondrial dynamics. The disruption dynamics closely related occurrence development DCM. Mitochondrial controlled by circadian clock show oscillation rhythm. This rhythm enables mitochondria respond changing demands different environments, but it disordered In this review, we summarize significant role clock-controlled etiology DCM hope play certain enlightening treatment

Language: Английский

Citations

12
MiR-21-3p inhibitor exerts myocardial protective effects by altering macrophage polarization state and reducing excessive mitophagy DOI Creative Commons
Yujing Huang,

Ya-Lin Huang,

Zhaoling Cai

et al.

Communications Biology, Journal Year: 2024, Volume and Issue: 7(1)

Published: Oct. 22, 2024

Chronic heart failure (CHF) is closely associated with inflammation and mitochondrial dysfunction in cardiomyocytes. This study attempts to investigate the effects of microRNA-21-3p (miR-21-3p) on macrophage polarization mitophagy CHF. Here we found miR-21-3p was upregulated CHF negatively correlated carnitine palmitoyl transferase 1A (CPT1A). L-palmitoyl (L-PC) exacerbated isoproterenol (ISO)-induced myocardial structural disruption fibrosis rats, which by miR-21-3p. Mechanistically, accelerated M1 polarization. Both inhibitor CPT1A overexpression suppressed mitophagy. The inhibition reversed MiR-21-3p targeted mRNA co-localized protein In co-culture system macrophages H9c2 cells, mimics cells promoted polarization, whereas reduced phenotype. cell damage. These findings support potential therapeutic targeting regulate inducing Binding fatty acid metabolism-related target gene affects development chronic failure.

Language: Английский

Citations

4