Pulmonary arterial hypertension (PAH) is being redefined by molecular biology. Once viewed mainly as a disorder of excessive blood-vessel constriction, the disease is now understood as a progressive process involving vascular remodeling, immune activation, metabolic disruption, and inherited susceptibility. A review published online on June 17, 2026, in the Chinese Medical Journal describes how these interacting mechanisms are reshaping PAH research and opening the door to treatments designed not only to relieve symptoms, but also to alter the disease itself.

PAH is a rare and potentially fatal condition in which the small arteries carrying blood through the lungs become narrowed and structurally damaged. As resistance within the pulmonary circulation rises, the right side of the heart must pump harder to maintain blood flow. Over time, the right ventricle can enlarge, weaken, and fail. Current therapies have improved survival, but many patients continue to experience progressive disease, limited exercise capacity, and an uncertain long-term outlook. The new review was conducted by Dr. Taeil Yang of Gil Medical Center at Gachon University College of Medicine and Professor Wook-Jin Chung of the Gachon Cardiovascular Research Institute in the Republic of Korea.

The authors explain that PAH develops through a complex interaction among several types of cells in the pulmonary circulation. Endothelial cells, which form the inner lining of blood vessels, normally regulate vessel diameter, blood flow, clotting, and repair. In PAH, these cells become dysfunctional and can produce excessive vasoconstrictors while reducing protective signals such as nitric oxide and prostacyclin. Endothelial injury also promotes the recruitment of inflammatory cells and stimulates neighboring smooth-muscle cells and fibroblasts to multiply. The resulting changes thicken the vessel wall and progressively reduce the space available for blood flow.

Inflammation is another central feature of this transformation. T cells, B cells, macrophages, and other immune cells can accumulate around pulmonary arteries, releasing cytokines and growth factors that sustain vascular injury. Rather than being a temporary response to damage, this immune activity may become chronic, reinforcing the abnormal behavior of vascular cells. The review emphasizes that immune signaling is closely connected to endothelial dysfunction and tissue remodeling, suggesting that PAH cannot be fully understood by studying blood-vessel tone alone.

The metabolism of pulmonary vascular cells also changes as the disease advances. Under normal conditions, mitochondria generate much of the energy required for cellular function through oxidative phosphorylation. In PAH, endothelial and smooth-muscle cells may shift toward glycolysis, a pattern resembling the “Warburg effect” observed in cancer. This metabolic reprogramming allows cells to generate energy rapidly while supporting biosynthesis and proliferation. It can also increase resistance to programmed cell death, enabling abnormal cells to persist within the vessel wall. These changes help explain why pulmonary arteries can continue remodeling even when vasoconstriction is medically controlled.

Genetic research has provided some of the strongest evidence that PAH is driven by specific biological pathways. Variants in BMPR2, the gene most commonly associated with heritable PAH, can impair signaling involved in vascular growth, repair, and cell survival. Other genes linked to PAH include SOX17, TBX4, and KCNK3. Several of these genes influence the bone morphogenetic protein, or BMP, pathway and its relationship with transforming growth factor beta, known as TGF-β. When this signaling network is disrupted, the balance between controlled growth and abnormal proliferation can shift, increasing susceptibility to pulmonary vascular disease. Genetic risk, however, is not destiny: environmental exposures, inflammation, infections, hormonal influences, and other biological triggers may determine whether disease develops and how rapidly it progresses.

These discoveries are already influencing treatment strategies. Traditional PAH medicines primarily target pathways that regulate vascular constriction, including endothelin, nitric oxide, and prostacyclin signaling. Newer approaches aim deeper at the mechanisms driving vascular remodeling. Sotatercept has attracted particular attention because it acts on signaling within the BMP/TGF-β superfamily and is designed to restore a healthier balance between growth-promoting and growth-inhibiting signals. By targeting the biology of vessel-wall remodeling rather than simply dilating arteries, the therapy represents a shift toward disease modification. Researchers are also studying seralutinib, which targets growth-factor and platelet-derived growth-factor signaling, as well as immune-directed treatments such as tocilizumab and rituximab. Metabolism-focused therapies remain another active area of investigation.

The review also highlights the growing importance of multi-omics research. Genomics can reveal inherited variants, while transcriptomics shows which genes are active in diseased tissue. Proteomics measures changes in proteins and signaling molecules, and metabolomics captures the chemical products of altered cellular pathways. Combining these layers may reveal why patients with apparently similar clinical diagnoses can have very different disease trajectories or responses to therapy. Such information could eventually help physicians classify patients according to molecular subtypes, identify biomarkers before irreversible vascular damage occurs, and select treatments according to the dominant mechanism in each individual.

Professor Chung argues that the most promising future for PAH depends on connecting laboratory discoveries with carefully designed translational studies and clinical trials. That challenge is substantial because the disease involves multiple interacting cell types and pathways, and because tissue samples from the pulmonary circulation are difficult to obtain. Nevertheless, the expanding molecular framework is changing the goals of treatment. Instead of focusing exclusively on lowering pulmonary artery pressure, researchers are seeking ways to repair endothelial dysfunction, restrain immune activity, normalize cellular metabolism, and reverse pathological remodeling. The field is moving toward precision medicine in which genetic and molecular information may guide therapy, offering patients the possibility of longer-lasting control and, ultimately, recovery of healthier pulmonary vascular function.

Subject of Research: Pulmonary arterial hypertension and its molecular mechanisms and emerging treatments

Article Title: Pulmonary arterial hypertension from a translational perspective: Bridging pathophysiology and treatment

News Publication Date: 17-Jun-2026

Web References: https://doi.org/10.1097/CM9.0000000000004137

References: Chinese Medical Journal, DOI: 10.1097/CM9.0000000000004137

Image Credits: Chinese Medical Journal

Keywords: Pulmonary arterial hypertension; PAH; BMPR2; SOX17; TBX4; KCNK3; BMP signaling; TGF-β; vascular remodeling; endothelial dysfunction; inflammation; metabolic reprogramming; sotatercept; seralutinib; precision medicine

Jonathan Wells’s review was important, but it only scratches the surface of information in biology outside of the DNA.

Source

Baker's yeast is one of biotechnology's most important microorganisms. It has long been used to leaven bread and ferment beer. More recently, advances in synthetic biology have enabled engineered yeast to convert sugar into a wide range of products, including medicines, fuels and industrial chemicals. Yet even well-engineered yeast cells can be difficult to control in a precise and timely way.

Baker's yeast is one of biotechnology's most important microorganisms. It has long been used to leaven bread and ferment beer. More recently, advances in synthetic biology have enabled engineered yeast to convert sugar into a wide range of products, including medicines, fuels and industrial chemicals. Yet even well-engineered yeast cells can be difficult to control in a precise and timely way.

Intelligence is an energetically expensive luxury – as the rise of artificial intelligence has reminded us. The human brain is no exception. Comprising roughly 2% of the body weight, it uses one fifth the body’s energy in the resting state – compared with less than half of this in non-human primates. A five-year-old child devotes […]

The post Fruit And Honey Fueled the Early Evolution of The Human Brain appeared first on Knowridge Science Report.

Every living cell, from the simplest bacterium to a human neuron, relies on the same basic machinery to read, interpret, and use its DNA. This molecular machinery is so fundamental that life as we know it cannot exist without it. And because it is so essential, it has long been a target for drugs; it shuts down a bacterium's ability to access its own genes and it quickly dies.

The global expansion of chicken farming has created conditions that allow Campylobacter to spread, mix and adapt more readily. Commercial poultry farms now hold billions of chickens, creating a vast habitat where bacteria can move, mix and adapt. An analysis from the Ineos Oxford Institute for Antimicrobial Research at the University of Oxford found that [...]

Study reveals how contamination can increase within colonies. Inside a honeybee colony, worker bees act as living filters. They intercept much of the pesticide contamination entering the hive, helping shield the queen and the developing young she produces. But when exposure continues and that protective system begins to fail, the queen may redirect the chemical [...]

When a wound does not heal properly, it leaves a scar. Similarly, mutations—which are permanent changes to genetic code—are often the result of damaged DNA that has not been properly repaired. Mutations can impede the function of genes and lead to disease and aging, but they are also the source of genetic variation, which allows new traits to emerge and facilitates the evolutionary process. Scientists still do not fully understand why some damaged DNA segments are successfully repaired while others are not.

When a wound does not heal properly, it leaves a scar. Similarly, mutations—which are permanent changes to genetic code—are often the result of damaged DNA that has not been properly repaired. Mutations can impede the function of genes and lead to disease and aging, but they are also the source of genetic variation, which allows new traits to emerge and facilitates the evolutionary process. Scientists still do not fully understand why some damaged DNA segments are successfully repaired while others are not.

A shortage of one common nutrient could help cancer cells and viruses hide from the immune system. Researchers at Rockefeller University found that a shortage of arginine, an amino acid obtained from food and produced by the body, can interrupt the cellular machinery needed to make MHC-I proteins. These proteins act as a surveillance system, [...]

Photosynthetic microorganisms can use light energy to convert carbon dioxide into useful compounds under mild, environmentally compatible conditions. However, many current photosynthetic production systems rely on cells growing freely in large volumes of liquid. This creates a substantial demand for water and requires extensive mixing to keep the cells evenly distributed and exposed to light, increasing the resource and energy requirements of the process.

For most healthy people, Cryptococcus is an unnoticed infection. The immune system walls it off in the lungs and keeps it dormant for life. But in patients undergoing cancer chemotherapy, recovering from an organ transplant, living with HIV or taking newer immunosuppressing drugs for autoimmune disease, the fungus can reactivate, spread to the brain and cause meningitis.

The study's authors mean well. But the technology is unnerving.

For decades, astronomers have assumed that the Martian surface froze solid around 3 billion years ago and has stayed that way ever since. If this were really the case, any liquid water would have long since either been locked away underground or lost to space.

Dinosaurs evolved into some of the largest animals ever to walk the Earth, but a new mathematical model suggests that early mammals may have crowded them out of the ecological niches reserved for the smallest creatures.

The post Why Were There No Tiny Non-Avian Dinosaurs? Mammals May Have Been to Blame appeared first on Sci.News: Breaking Science News.

Third Way and EES thinking shows that mainstream science is moving on a compass heading that is right in the direction of intelligent design.

Source

Any dog owner would tell you that their canine companions are attuned to their humans' emotional state and respond accordingly. Scientists have performed fMRI scans on dogs and identified a specific brain region that processes happy human facial expresses, like a smile, according to a new paper published in the journal iScience. They also found that dogs can tell the difference between negative facial expressions, specifically anger, sadness, and fear.

“Humans are really good at picking up small details on the face, and so are dogs,” said co-author Raúl Hernández-Pérez of the University of Vienna. “This makes dogs very interesting. By studying their brains, we can understand what adaptations have developed to support their remarkable social and emotional understanding of humans.”

Prior behavioral studies have shown that dogs are sensitive to emotion in human faces. Dogs will, for example, choose a box their human has identified with a happy expression over one the human treats with fear or disgust. Past fMRI studies found that an area in the canine left temporal cortex showed a stronger response to human faces compared to dog faces, as well as a greater response in the caudate, hippocampus, and amygdala to human faces showing emotion versus neutral faces.

Read full article

Comments

© Laura V. Cuaya/CC BY-SA

Any dog owner would tell you that their canine companions are attuned to their humans' emotional state and respond accordingly. Scientists have performed fMRI scans on dogs and identified a specific brain region that processes happy human facial expresses, like a smile, according to a new paper published in the journal iScience. They also found that dogs can tell the difference between negative facial expressions, specifically anger, sadness, and fear.

“Humans are really good at picking up small details on the face, and so are dogs,” said co-author Raúl Hernández-Pérez of the University of Vienna. “This makes dogs very interesting. By studying their brains, we can understand what adaptations have developed to support their remarkable social and emotional understanding of humans.”

Prior behavioral studies have shown that dogs are sensitive to emotion in human faces. Dogs will, for example, choose a box their human has identified with a happy expression over one the human treats with fear or disgust. Past fMRI studies found that an area in the canine left temporal cortex showed a stronger response to human faces compared to dog faces, as well as a greater response in the caudate, hippocampus, and amygdala to human faces showing emotion versus neutral faces.

Read full article

Comments

© Laura V. Cuaya/CC BY-SA

Ancient animal waste may have helped fuel the development and diversification of early marine ecosystems. Tiny pellets of fossilized waste may preserve evidence of a major transformation in early animal life. An international study led by Flinders University proposes that excrement helped reshape ancient oceans during one of evolution’s most important turning points. The researchers [...]