Pulmonary involvement from animal toxins: the cellular mechanisms

Abstract Venomous animals and their venom have always been of human interest because, despite species differences, coevolution has made them capable of targeting key physiological components of our bodies. Respiratory failure from lung injury is one of the serious consequences of envenomation, and the underlying mechanisms are rarely discussed. This review aims to demonstrate how toxins affect the pulmonary system through various biological pathways. Herein, we propose the common underlying cellular mechanisms of toxin-induced lung injury: interference with normal cell function and integrity, disruption of normal vascular function, and provocation of excessive inflammation. Viperid snakebites are the leading cause of envenomation-induced lung injury, followed by other terrestrial venomous animals such as scorpions, spiders, and centipedes. Marine species, particularly jellyfish, can also inflict such injury. Common pulmonary manifestations include pulmonary edema, pulmonary hemorrhage, and exudative infiltration. Severe envenomation can result in acute respiratory distress syndrome. Pulmonary involvement suggests severe envenomation, thus recognizing these mechanisms and manifestations can aid physicians in providing appropriate treatment.

Research progress on cellular and molecular mechanism of keloids / 中国药理学通报

Keloid is a fibrous proliferative disease of the skin, and its pathological essence is excessive wound healing caused by excessive fibrosis. Its pathological mechanism is complex and unclear. At present, it is believed that the cellular mechanism of keloids mainly involves inflammatory cells and fibrosis-related cells, as well as cytokines such as growth factors, interleukins, tumor necrosis factor, and matrix metalloproteinase; the molecular mechanism mainly involves TGF-p/Smad pathway, NF-Mo- lecular mechanisms such as kB pathway, STAT3 signaling pathway, MAPK signaling pathway, and focal adhesion kinase. This article reviews the latest research progress on the pathological mechanism of keloids from the perspectives of cells, cytokines, and molecular signaling pathways.

Systemic and cellular responses to intermittent hypoxia relevance to recurrent apnea syndrome / 复旦学报（医学版）

Patients with sleep-disordered breathing with recurrent apneas exhibit autonomic dysfunction including elevated sympathetic nerve activity (SNA) and hypertension.Studies on experimental animals show that chronic intermittent hypoxia (CIH) resulting from recurrent apneas is a major stimulus for evoking autonomic dysfunction.In rodent models,CIH enhances arterial chemoreflex function in part due to enhanced carotid body sensitivity to hypoxia.The enhanced chemo-reflex leads to elevated sympathetic nerve activity.Recent studies suggest that transcriptional changes involving hypoxiainducible factor-1 and 2 (HIF-1,HIF-2) and the resulting reactive oxygen species-mediated signaling are critical cellular mechanisms underlying the chemoreflex-mediated excitation of sympathetic nervous system by CIH.