Inhaled nanoparticle (NP) therapy poses intricate challenges in clinical and pharmacodynamic realms. Recent strides have revolutionized NP technology by enabling the incorporation of diverse molecules, thus circumventing systemic clearance mechanisms and enhancing drug effectiveness while mitigating systemic side effects. Despite the established success of systemic NP delivery in oncology and other disciplines, the exploration of inhaled NP therapies remains relatively nascent. NPs loaded with bronchodilators or anti-inflammatory agents exhibit promising potential for precise distribution throughout the bronchial tree, offering targeted treatment for respiratory diseases. This article conducts a comprehensive review of NP applications in respiratory medicine, highlighting their merits, ranging from heightened stability to exacting lung-specific delivery. It also explores cutting-edge technologies optimizing NP-loaded aerosol systems, complemented by insights gleaned from clinical trials. Furthermore, the review examines the current challenges and future prospects in NP-based therapies. By synthesizing current data and perspectives, the article underscores the transformative promise of NP-mediated drug delivery in addressing chronic conditions such as chronic obstructive pulmonary disease, a pressing global health concern ranked third in mortality rates. This overview illuminates the evolving landscape of NP inhalation therapies, presenting optimistic avenues for advancing respiratory medicine and improving patient outcomes.

The renin–angiotensin–aldosterone system (RAAS) plays a central role in cardiovascular and renal homeostasis and is increasingly recognized for its broad immunomodulatory effects. Pharmacological RAAS inhibition, primarily via angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs), has demonstrated therapeutic value beyond its use in hypertension and heart failure, extending to autoimmune, infectious, oncologic, and neurodegenerative conditions. ACEIs and ARBs modulate both innate and adaptive immune responses through Ang II-dependent and -independent mechanisms, influencing macrophage polarization, T-cell differentiation, cytokine expression, and antigen presentation. Notably, ACEIs exhibit Ang II-independent effects by enhancing antigen processing and regulating amyloid-β metabolism, offering potential neuroprotective benefits in Alzheimer’s disease. ARBs, particularly telmisartan and candesartan, provide additional anti-inflammatory effects via PPARγ activation. In cancer, RAAS inhibition affects tumor growth, angiogenesis, and immune surveillance, with ACEIs and ARBs showing distinct yet complementary impacts on tumor microenvironment modulation and chemotherapy cardioprotection. Moreover, ACEIs have shown promise in autoimmune myocarditis, colitis, and diabetic nephropathy by attenuating inflammatory cytokines. While clinical evidence supports the use of centrally acting ACEIs to treat early cognitive decline, further investigation is warranted to determine the long-term outcomes across disease contexts. These findings highlight the evolving role of RAAS inhibitors as immunomodulatory agents with promising implications across multiple systemic pathologies.

Since the first cases of severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2) infection, there have been challenges recognizing the clinical features of SARS‑CoV‑2 and identifying therapeutic options. This has been compounded by viral mutations that affect clinical response and primary epidemiological indicators. Multiple variants of SARS‑CoV‑2 have been identified and classified on the basis of nomenclature implemented by scientific organizations and the World Health Organisation (WHO). A total of five variants of concern (VOCs) have been identified to date. The present study aimed to analyse clinical and epidemiological features of each variant. Based on these characteristics, predictions were made about potential future evolution. Considering the time and location of SARS‑CoV‑2 VOC emergence, it was hypothesised that mutations were not due to pressure caused by the vaccines introduced in December 2020 but were dependent on natural characteristics of the virus. In the process of adapting to the human body, SARS‑CoV‑2 is expected to undergo evolution to become more contagious but less deadly. SARS‑CoV‑2 was hypothesized to continue spread through isolated epidemic outbreaks due to the unimmunized population, mostly unvaccinated children and adults, and for coronaviruses to continue to present a public health problem.

The renin-angiotensin system (RAS) is one of the biggest challenges of cardiovascular medicine. The significance of the RAS in the chronic progression of SARS-CoV-2 infection and its consequences is one of the topics that are currently being mostly discussed. SARS-CoV-2 undermines the balance between beneficial and harmful RAS pathways. The level of soluble ACE2 and membrane-bound ACE2 are both upregulated by the endocytosis of the SARS-CoV-2/ACE2 complex and the tumor necrosis factor (TNF)-α-converting enzyme (ADAM17)-induced cleavage. Through the link between RAS and the processes of proliferation, the processes of fibrous remodelling of the myocardium are initiated from the acute phase of the disease, continuing into the long COVID stage. In the long term, RAS dysfunction may cause an impairment of its beneficial effects leading to thromboembolic processes and a reduction in perfusion of target organs. The main aspects of ACE2—a key pathogenic role in COVID-19 as well as the mechanisms of RAS involvement in COVID cardiovascular injuries are studied. Therapeutic directions that can be currently anticipated in relation to the various pathogenic pathways of progression of cardiovascular damage in patients with longCOVID have also been outlined.

Chronic obstructive pulmonary disease (COPD) is one of the most challenging chronic disease nowadays due to increased morbidity and mortality, despite the multiple new therapies included in the therapeutic scheme. A possible cause may be insufficient approach to thromboembolic risk in these patients, scientific data being so far insufficient and relatively controversial. Areas covered: anticoagulant therapy is used mainly during severe exacerbations. There are data that have shown that therapy with low weight heparins injectable anticoagulants causes not only a reduction in thromboembolic risk but also an improvement in respiratory function parameters. Expert opinion: a number of COPD phenotypes are more prone to procoagulant status and thrombus formation. A layered approach to COPD patients in terms of antithrombotic prophylaxis is needed. Although current published clinical data have not provided irrefutable evidence, possibly due to the relatively heterogeneous approach to inclusion criteria, the frequent identification of autopsy holes in patients with COPD suggests that the high risk of mortality is due to specific bronchopulmonary changes and pulmonary embolism.

Obstructive sleep apnoea (OSA), also characterised by hypoxia-related sleep- fragmentation, has been studied in relation to depression and serum testosterone deficit. In middle-aged men, it has been reported the association between depressive mood and low serum testosterone level; however, no data are available about this association in OSA patients. Therefore, the aim of this study was to investigate in adult obese males, affected by severe OSA, the relationship between serum testosterone concentration and depressive symptoms, in order to identify among all measured parameters (serum testosterone morning concentration, polysomnography parameters, body mass index, Epworth Sleepiness Scale) those predictors for OSA-related depression. Forty patients diagnosed with severe OSA and forty subjects for the control-matched group were enroled in the study. The results indicated that the serum testosterone in OSA group was significantly lower than in controls. In addition, the OSA group presented a level of depression although moderate, yet significantly higher than controls. Furthermore, a statistically significant inverse correlation has been found between serum testosterone level and depressive symptoms. Among all variables, serum testosterone level was shown to be the only independent variable significantly predictor for depression in OSA patients.