Scoping review of post-TB pulmonary vascular disease: Proceedings from the 2nd International Post-Tuberculosis Symposium.

Tuberculosis (TB) may cause significant long-term cardiorespiratory complications, of which pulmonary vascular disease is most under-recognized. TB is rarely listed as a cause of pulmonary hypertension (PH) in most PH guidelines, yet PH may develop at various stages in the time course of TB, from active infection through to the post-TB period. Predisposing risk factors for the development of PH are likely multifactorial, involving active TB disease and post-TB lung disease (PTLD), host-related and environment-related factors.

Cytotoxic properties, glycolytic effects and high-resolution respirometry mitochondrial activities of Eriocephalus racemosus against MDA-MB 231 triple-negative breast cancer.

Introduction: Triple-negative breast cancer (TNBC) represents a significant global health crisis due to its resistance to conventional therapies and lack of specific molecular targets. This study explored the potential of Eriocephalus racemosus (E. racemosus) as an alternative treatment for TNBC.

Post-tuberculosis lung disease and inflammatory role players: can we characterise the myriad inflammatory pathways involved to gain a better understanding?

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.

Gut microbiota crosstalk mechanisms are key in pulmonary hypertension: The involvement of melatonin is instrumental too.

The microbiota refers to a plethora of microorganisms with a gene pool of approximately three million, which inhabits the human gastrointestinal tract or gut. The latter, not only promotes the transport of nutrients, ions, and fluids from the lumen to the internal environment but is linked with the development of diseases including coronary artery disease, heart failure, and lung diseases. The exact mechanism of how the microbiota achieves crosstalk between itself and distant organs/tissues is not clear, but factors released to other organs may play a role, like inflammatory and genetic factors, and now we highlight melatonin as a novel mediator of the gut-lung crosstalk.

The prevalence of pulmonary hypertension after successful tuberculosis treatment in a community sample of adult patients.

There are an estimated 155 million survivors of tuberculosis (TB). Clinical experience suggests that post tuberculosis lung disease (PTLD) is an important cause of Group 3 pulmonary hypertension (PH). However, TB is not listed as a cause of PH in most guidelines.

Reviewing the suitability of mitochondrial transplantation as therapeutic approach for pulmonary hypertension in the era of personalized medicine.

Pulmonary hypertension (PH) is a fatal disease, defined as a mean pulmonary artery pressure ≥25 mmHg. It is caused, in part, by mitochondrial dysfunction. Among the various biological therapies proposed to rescue mitochondrial dysfunction, evidence going back as far as 2009 suggests that mitochondrial transplantation is an alternative.

Melatonin against pulmonary arterial hypertension: is it ready for testing in patients?

Pulmonary arterial hypertension (PAH) is a fatal disease defined as a mean pulmonary artery pressure exceeding 25 mmHg when diagnosed with right heart catheterisation. Its pathophysiology involves multiple molecular pathways, including key components leading to an inflammatory and oxidative stress environment that ultimately causes right ventricular hypertrophy and failure. Compared to the developed world, the overall PAH prevalence is higher in developing countries, including Africa, where it is mostly associated with left heart disease, obstructive/restrictive pulmonary disease, HIV and rheumatic heart disease.

Pulmonary hypertension in majority countries: opportunities amidst challenges.

Purpose Of Review: Pulmonary hypertension is a deadly disease, the causes of which vary between geographical regions. Eighty four percentage of the world's population lives in majority countries (also called low-income and middle-income countries), yet data on pulmonary hypertension in these settings are proportionally scarce. This article provides a review of pulmonary hypertension in majority countries, focusing in detail on the most common causes in these regions, and highlights contextual challenges faced.

Determination of HIV status and identification of incident HIV infections in a large, community-randomized trial: HPTN 071 (PopART).

Introduction: The HPTN 071 (PopART) trial evaluated the impact of an HIV combination prevention package that included "universal testing and treatment" on HIV incidence in 21 communities in Zambia and South Africa during 2013-2018. The primary study endpoint was based on the results of laboratory-based HIV testing for> 48,000 participants who were followed for up to three years. This report evaluated the performance of HIV assays and algorithms used to determine HIV status and identify incident HIV infections in HPTN 071, and assessed the impact of errors on HIV incidence estimates.

Making a case for metallothioneins conferring cardioprotection in pulmonary hypertension.

Pulmonary hypertension (PH) is defined as elevated mean pulmonary artery pressure secondary to e.g. congenital heart disease and chronic obstructive pulmonary disease.

Pulmonary arterial hypertension and the potential roles of metallothioneins: A focused review.

The pathophysiology of pulmonary arterial hypertension (PAH) is underlined by cell proliferation and vasoconstriction of pulmonary arterioles this involves multiple molecular factors or proteins, but it is not clear what the exact roles of these factors/proteins are. In addition, there may be other factors/proteins that have not been identified that contribute to PAH pathophysiology. Therefore, research has focused on investigating novel role players, in order to facilitate a better understanding of how PAH develop.

Melatonin in Heart Failure: A Promising Therapeutic Strategy?

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.

Coordinated autophagy modulation overcomes glioblastoma chemoresistance through disruption of mitochondrial bioenergetics.

Glioblastoma Multiforme (GBM) is known to be one of the most malignant and aggressive forms of brain cancer due to its resistance to chemotherapy. Recently, GBM was found to not only utilise both oxidative phosphorylation (OXPHOS) and aerobic glycolysis, but also depend on the bulk protein degradation system known as macroautophagy to uphold proliferation. Although autophagy modulators hold great potential as adjuvants to chemotherapy, the degree of upregulation or inhibition necessary to achieve cell death sensitisation remains unknown.

Melatonin therapy for blunt trauma and strenuous exercise: A mechanism involving cytokines, NFκB, Akt, MAF and MURF-1.

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.

Natural Antioxidants as Potential Therapy, and a Promising Role for Melatonin Against Pulmonary Hypertension.

Plasma and serum samples, and lung/heart tissue of pulmonary hypertension (PH) patients and animal models of PH display elevated oxidative stress. Moreover, the severity of PH and levels of oxidative stress increase concurrently, which suggests that oxidative stress could be utilized as a biomarker for PH progression. Accumulating evidence has well established that oxidative stress is also key role player in the development of PH.

Review of a causal role of fructose-containing sugars in myocardial susceptibility to ischemia/reperfusion injury.

In 2012, the World Health Organization Global Status Report on noncommunicable diseases showed that 7.4 million deaths were due to ischemic heart disease. Consequently, cardiovascular disease is a significant health burden, especially when partnered with comorbidities such as obesity, metabolic syndrome, and type 2 diabetes mellitus.

Novel putative pharmacological therapies to protect the right ventricle in pulmonary hypertension: a review of current literature.

Pulmonary hypertension (PH) is defined by elevated mean pulmonary artery pressure following the pathological remodelling of small pulmonary arteries. An increase in right ventricular (RV) afterload results in RV hypertrophy and RV failure. The pathophysiology of PH, and RV remodelling in particular, is not well understood, thus explaining, at least in part, why current PH therapies have a limited effect.

Melatonin protects against uric acid-induced mitochondrial dysfunction, oxidative stress, and triglyceride accumulation in CC myotubes.

Excess uric acid has been shown to induce oxidative stress, triglyceride accumulation, and mitochondrial dysfunction in the liver and is an independent predictor of type-2 diabetes. Skeletal muscle plays a dominant role in type 2 diabetes and presents a large surface area to plasma uric acid. However, the effects of uric acid on skeletal muscle are underinvestigated.

Uric acid and transforming growth factor in fructose-induced production of reactive oxygen species in skeletal muscle.

The consumption of fructose, a major constituent of the modern diet, has raised increasing concern about the effects of fructose on health. Research suggests that excessive intake of fructose (>50 g/d) causes hyperuricemia, insulin resistance, mitochondrial dysfunction, de novo lipogenesis by the liver, and increased production of reactive oxygen species (ROS) in muscle. In a number of tissues, uric acid has been shown to stimulate the production of ROS via activation of transforming growth factor β1 and NADPH (nicotinamide adenine dinucleotide phosphate) oxidase 4.

Measurement of β-oxidation capacity of biological samples by respirometry: a review of principles and substrates.

Oxidation of fatty acids is a major source of energy in the heart, liver, and skeletal muscle. It can be measured accurately using respirometry in isolated mitochondria, intact cells, and permeabilized cells or tissues. This technique directly measures the rate of oxygen consumption or flux at various respiratory states when appropriate substrates, uncouplers, and inhibitors are used.

Melatonin as a preventive and curative therapy against pulmonary hypertension.

Pulmonary hypertension (PH) is characterized by elevated pulmonary arterial pressure, which leads to right ventricular (RV) hypertrophy and failure. The pathophysiological mechanisms of PH remain unclear but oxidative stress is believed to contribute to RV dysfunction. Melatonin is a powerful antioxidant and is cardioprotective against ischemia-reperfusion injury and hypertension.

A comprehensive review: the evolution of animal models in pulmonary hypertension research; are we there yet?

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.