Despite advances in treatments and therapies, cardiovascular diseases (CVDs) remain one of the leading causes of death worldwide. The discovery that most of the human genome, although transcribed, does not encode proteins was crucial for focusing on the potential of long non-coding RNAs (lncRNAs) as essential regulators of cell function at the epigenetic, transcriptional, and post-transcriptional levels. This class of non-coding RNAs is related to the pathophysiology of the cardiovascular system. The different expression profiles of lncRNAs, in different contexts of CVDs, change a great potential in their use as a biomarker and targets of therapeutic intervention. Furthermore, regular physical exercise plays a protective role against CVDs; on the other hand, little is known about its underlying molecular mechanisms. In this review, we look at the accumulated knowledge on lncRNAs and their functions in the cardiovascular system, focusing on the cardiovascular pathology of arterial hypertension, coronary heart disease, acute myocardial infarction, and heart failure. We discuss the potential of these molecules as biomarkers for clinical use, their limitations, and how the manipulation of the expression profile of these transcripts through physical exercise can begin to be suggested as a strategy for the treatment of CVDs.

Cardiovascular and metabolic diseases such as hypertension, type 2 diabetes, and obesity develop long-term fibrotic processes in the heart, promoting pathological cardiac remodeling, including after myocardial infarction, reparative fibrotic processes also occur. These processes are regulated by many intracellular signaling pathways that have not yet been completely elucidated, including those associated with microRNA (miRNA) expression. miRNAs are small RNA transcripts (18–25 nucleotides in length) that act as posttranscriptionally regulators of gene expression, inhibiting or degrading one or more target messenger RNAs (mRNAs), and proven to be involved in many biological processes such as cell cycle, differentiation, proliferation, migration, and apoptosis, directly affecting the pathophysiology of several diseases, including cardiac fibrosis. Exercise training can modulate the expression of miRNAs and it is known to be beneficial in various cardiovascular diseases, attenuating cardiac fibrosis processes. However, the signaling pathways modulated by the exercise associated with miRNAs in cardiac fibrosis were not fully understood. Thus, this review aims to analyze the expression of miRNAs that modulate signaling pathways in cardiac fibrosis processes that can be regulated by exercise training.

Aerobic exercise training (ET) produces beneficial adaptations in skeletal muscles, including angiogenesis. The renin–angiotensin system (RAS) is highly involved in angiogenesis stimuli. However, the molecular mechanisms underlying capillary growth in skeletal muscle induced by aerobic ET are not completely understood. This study aimed to investigate the effects of volume-dependent aerobic ET on skeletal muscle angiogenesis involving the expression of miRNAs-27a and 27b on RAS and oxidant–antioxidant balance. Eight-week-old female Wistar rats were divided into three groups: sedentary control (SC), trained protocol 1 (P1), and trained protocol 2 (P2). P1 consisted of 60 min/day of swimming, 5×/week, for 10 weeks. P2 consisted of the same protocol as P1 until the 8th week, but in the 9th week, rats trained 2×/day, and in the 10th week, trained 3×/day. Angiogenesis and molecular analyses were performed in soleus muscle samples. Furthermore, to establish ET-induced angiogenesis through RAS, animals were treated with an AT1 receptor blocker (losartan). Aerobic ET promoted higher VO₂ peak and exercise tolerance values. In contrast, miRNA-27a and -27b levels were reduced in both trained groups, compared with the SC group. This was in parallel with an increase in the ACE1/Ang II/VEGF axis, which led to a higher capillary-to-fiber ratio. Moreover, aerobic ET induced an antioxidant profile increasing skeletal muscle SOD2 and catalase gene expression, which was accompanied by high nitrite levels and reduced nitrotyrosine concentrations in the circulation. Additionally, losartan treatment partially re-established the miRNAs expression and the capillary-to-fiber ratio in the trained groups. In summary, aerobic ET promoted angiogenesis through the miRNA-27a/b–ACE1/Ang II/VEGF axis and improved the redox balance. Losartan treatment demonstrates the participation of RAS in ET-induced vascular growth. miRNAs and RAS components are promising potential targets to modulate angiogenesis for combating vascular diseases, as well as potential biomarkers to monitor training interventions and physical performance.

Sarcopenia has been defined as the loss of skeletal muscle mass and strength that occurs with advancing age and has also been related to many metabolic diseases. In late stages, sarcopenia precedes cachexia, defined as a multifactorial syndrome characterized by an ongoing skeletal muscle wasting, with or without loss of fat mass, associated with poor prognosis in diseases, worsening quality of life and survival. Heart failure and cancer-associated cachexia represents a progressive involuntary weight loss and is mainly the result of an imbalance in the muscle protein synthesis and degradation, inflammation, and oxidative stress, causing muscle wasting. Importantly, both diseases are still the main causes of death worldwide and the molecular basis of cachexia is still poorly understood. Recently, non-coding RNAs have been described to regulate the cardiac and cancer-associated cachexia. On the other hand, exercise training is a promising ally in slowing down cachexia and improving the quality of life of patients. New studies demonstrate that exercise training, acting through non-coding RNAs, may be able to mitigate muscle wasting, as protein turnover, mitochondrial biogenesis, and antioxidant capacity improvement. This review will therefore discuss the molecular mechanisms associated with the muscle wasting in both cardiac and cancer cachexia, as well as highlighting the effects of exercise training in attenuating the loss of muscle mass in these specific conditions.

Durante os últimos anos, um aumento significativo de novos casos de câncer tem sido observado, e com isto a doença e inúmeros métodos para a redução dos efeitos colaterais ao tratamento vêm sendo cada vez mais estudados. A fadiga oncológica é um fator predominante entre os portadores desta doença. O objetivo geral deste estudo foi analisar se o exercí­cio fí­sico promove uma redução no quadro crônico de fadiga. Trata-se de estudo de caráter bibliográfico que utilizou as bases de dados: Pubmed, Scielo e Google Acadêmico, e contou com os descritores em inglês e português: Cancer, physical exercise, immune system e fatigue oncology. A busca teve como critério de inclusão e exclusão as leituras dos resumos e foram eliminados aqueles que não corresponderam com o objetivo da pesquisa, foram excluí­dos também aqueles artigos que eram obtidos de forma paga. Concluiu-se, após o desenvolvimento do estudo, que o exercí­cio praticado de forma orientada e bem realizada traz benefí­cios na redução da fadiga e melhora na qualidade de vida dos pacientes com esta enfermidade.