Monash University led researchers discover potential breakthrough in hypertension treatment

New Delhi: A team of scientists from Monash University and the Baker Heart and Diabetes Institute in Melbourne has revealed promising findings in the quest to treat organ damage caused by hypertension, commonly known as high blood pressure. Their research marks a significant step forward in addressing the severe health complications associated with this prevalent condition.

Hypertension can lead to damaging effects on vital organs such as the heart, kidneys, and blood vessels, often resulting in conditions like enlarged hearts and weakened vessels. Despite existing treatments, which focus on controlling blood pressure, there remains a critical gap in effectively managing hypertension-induced organ damage.

The breakthrough centers on a novel therapeutic approach involving a small-molecule pro-resolving activator known as ‘compound17b’ (Cmpd17b), developed and studied extensively at the Monash Institute of Pharmaceutical Sciences (MIPS). Researchers have demonstrated that Cmpd17b not only protects against heart attacks but also shows promise in mitigating the detrimental effects of hypertension-induced organ damage.

Through a rigorous investigation combining animal models and human studies, the study, funded in part by the National Heart Foundation of Australia and other research grants discovered that Cmpd17b activates the formyl peptide receptor (FPR) family. This activation plays a crucial role in regulating inflammation, a key driver of organ damage in hypertension. By targeting these receptors, Cmpd17b emerges as a potent therapeutic agent capable of safeguarding vital organs from the ravages of high blood pressure.

Jaideep Singh, a PhD candidate at MIPS and co-first author of the study published in Cardiovascular Research, expressed, “Organ damage is a pathological feature of hypertension, responsible for significant morbidity and mortality, however current drugs to treat hypertension are limited when it comes to treating hypertension-induced end-organ damage, so there is absolutely a need to resolve this.”

“Our team has shown, for the first time, that not only does Cmpd17b normalise structure and function of heart and blood vessels in hypertensive mice, there is also a clear correlation with human hypertension suggesting Cmpd17b might also be effective in clinical settings,” Singh added.

Professor Geoff Head AM, senior author and Head of the Neuropharmacology Laboratory at the Baker Institute emphasized, “FPRs are like bodyguards that control inflammation, a big problem in high blood pressure. As a team, it’s exciting to report that Cmpd17b, which activates these FPRs, could be a promising way to prevent and treat the damage high blood pressure does to our organs in the long run.”

Dr. Chengxue Helena Qin, corresponding author and MIPS lab head, highlighted “We found that Cmpd17b, a new type of medication, can reverse some of these changes and improve heart and blood vessel health. This suggests that similar treatments might work in people with high blood pressure too.”

Dr. Qin noted, “Using medications like Cmpd17b could offer a novel approach to addressing hypertension-related cardiovascular complications, potentially reversing organ damage. Combining Cmpd17b with existing treatments may yield even better outcomes in managing hypertension-related health challenges.”