Pulmonary hypertension (PH) is a disorder that develops as a result of remodeling of the pulmonary vasculature and is characterized by narrowing/obliteration of small pulmonary arteries, leading to increased mean pulmonary artery pressure and pulmonary vascular resistance. Subsequently, PH increases the right ventricular afterload, which leads to right ventricular hypertrophy and eventually right ventricular failure. The pathophysiology of PH is not fully elucidated, and current treatments have only a modest impact on patient survival and quality of life. Thus, there is an urgent need for improved treatments or a cure. The use of animal models has contributed extensively to the current understanding of PH pathophysiology and the investigation of experimental treatments. However, PH in current animal models may not fully represent current clinical observations. For example, PH in animal models appears to be curable with many therapeutic interventions, and the severity of PH in animal models is also believed to correlate poorly with that observed in humans. In this review, we discuss a variety of animal models in PH research, some of their contributions to the field, their shortcomings, and how these have been addressed. We highlight the fact that the constant development and evolution of animal models will help us to more closely model the severity and heterogeneity of PH observed in humans.

Heart failure is a multifactorial clinical syndrome characterized by the inability of the heart to pump sufficient blood to the body. Despite recent advances in medical management, poor outcomes in patients with heart failure remain very high. This highlights a need for novel paradigms for effective, preventive and curative strategies. Substantial evidence supports the importance of endogenous melatonin in cardiovascular health and the benefits of melatonin supplementation in various cardiac pathologies and cardiometabolic disorders. Melatonin plays a crucial role in major pathological processes associated with heart failure including ischemic injury, oxidative stress, apoptosis, and cardiac remodeling. In this review, available evidence for the role of melatonin in heart failure is discussed. Current challenges and possible limitations of using melatonin in heart failure are also addressed. While few clinical studies have investigated the role of melatonin in the context of heart failure, current findings from experimental studies support the potential use of melatonin as preventive and adjunctive curative therapy in heart failure.

Tuberculosis (TB) remains a global health threat, and even after successful TB treatment, a subset of patients develops serious long-term lung impairments, recently termed post-tuberculosis lung disease (PTLD). Much remains to be discovered, as PTLD as a post-TB disease is a developing field, still in its infancy. The pathogenesis of PTLD is not fully elucidated but has been linked to elevated inflammatory pathways. The complexity of PTLD makes it challenging to pinpoint the specific inflammatory pathways involved in its pathophysiology . Therefore, this paper provides a comprehensive review of inflammatory cytokines and their potential roles in PLTD, with a specific focus on interleukin 6 (IL-6), IL-1, IL-8, tumour necrosis factor-alpha (TNF-α), transforming growth factor beta (TGF-β) and C-Reactive Protein (CRP). We delve into PTLD pathology, discuss its impact on lung function and review risk factors for PTLD. In addition, we summarise the current gaps in knowledge, provide recommendations for measuring inflammatory biomarkers and propose potential directions for future studies. We propose that future studies measure a wide range of inflammatory markers in TB populations with and without PTLD. In addition, studies could isolate peripheral blood mononuclear cells from patient blood to try and identify possible impairments that could be correlated with a PTLD diagnosis. Given that the PTLD field is still in an early stage of development, a comprehensive inflammatory analysis may help to know which pathways are key in PTLD development, and this may ultimately help to predict patients who are at risk. More research is warranted.

Muscle injury occurs due to trauma, strenuous exercise or sports activities; most people affected are athletes. Ineffectively treated muscle injury can negatively affect sports careers and quality of life after retirement from sports. Reports have indicated that the current therapeutic management of muscle injury, particularly anti-inflammatory drugs, are not necessarily effective. Therefore, better therapies are required. Accumulating evidence has demonstrated melatonin’s potent antioxidant and anti-inflammatory actions against muscle pathology in sarcopenia or atrophy in systemic disease. However, the underlying mechanisms for the protective effect of melatonin in the context of trauma/strenuous exercise are multifactorial and not well described. This paper reviews data on melatonin’s impact on muscle injury and findings that points toward the mechanisms through which melatonin achieves muscle protection. The general concept described in this review is that melatonin inhibits NFκB, reduces cytokine expression, increases Akt that downregulates the ratio of MAF_BX and MURF-1 in order to limit the extent of muscle injury and promote muscle recovery post-injury. The work discussed in this review supports the notion that melatonin may be considered a possible therapy against trauma/sports related muscle injury. Inclusion of melatonin as a therapy in sports medicine could therefore provide a better treatment option for injured athletes and sports individuals.