Pulmonary hypertension (PH) is a serious cardiovascular disease caused by a variety of pathogenic factors, which is characterized by increased pulmonary vascular resistance (PVR) and progressive elevation of mean pulmonary artery pressure (mPAP). This disease can lead to right ventricular hypertrophy and, in severe cases, right heart failure and even death. Vascular remodeling—a pathological modification involving aberrant vasoconstriction, cell proliferation, apoptosis resistance, and inflammation in the pulmonary vascular system—is a significant pathological hallmark of PH and a critical process in its progression. Recent studies have found that vascular remodeling involves the participation of a diversity of cellular pathological alterations, such as the dysfunction of pulmonary artery endothelial cells (PAECs), the proliferation and migration of pulmonary artery smooth muscle cells (PASMCs), the phenotypic differentiation of pulmonary artery fibroblasts, the inflammatory response of immune cells, and pericyte proliferation. This review focuses on the mechanisms and the intercellular crosstalk of these cells in the PH process, emphasizing recent advances in knowledge regarding cellular signaling pathways, inflammatory responses, apoptosis, and proliferation. To develop better treatments, a list of possible therapeutic approaches meant to slow down certain biological functions is provided, with the aim of providing new insights into the treatment of PH by simplifying the intricacies of these complex connections. In this review, comprehensive academic databases such as PubMed, Embase, Web of Science, and Google Scholar were systematically searched to discuss studies relevant to human and animal PH, with a focus on vascular remodeling in PH.

Melasma is a commonly acquired hyperpigmentation disorder characterized by symmetrical facial macules, with a notably higher prevalence in women and individuals with darker skin tones. Its etiology involves a multifactorial interplay of genetic predisposition, ultraviolet radiation exposure, and hormonal factors. This review consolidates current evidence highlighting the instrumental roles of estrogen and progesterone in modulating melanogenesis. These hormones regulate melanocyte activity via genomic and non-genomic signaling pathways, impacting key enzymes and transcription factors critical to pigment synthesis. Furthermore, crosstalk between hormonal signaling cascades exacerbates hyperpigmentation, contributing to the development of melasma. Therapeutically, targeting endocrine pathways is a promising yet investigational approach, as long-term clinical data remain scarce. Interventions such as receptor modulators and metabolic inhibitors may offer potential for reducing melanin production. Elucidating these endocrine mechanisms provides essential insights for developing more effective and personalized therapeutic strategies for melasma.