Pub Date : 2026-01-08DOI: 10.1016/j.cophys.2026.100898
Wayne R Fitzgibbon
Plasma and tissue levels of angiotensin peptides are regulated by their formation and metabolism by peptidases. Aminopeptidases A and N process Ang II to Ang III and Ang III to Ang IV, respectively, peptides which may have the same physiological action as, or counterbalance the action of, Ang II. In this minireview, other pathways for the processing of both Ang I and Ang II by aminopeptidases will be outlined. Further, the differential processing of Ang I and Ang II by different cell types comprising the renal glomerulus will be discussed. Importantly, by playing a role in the regulation of Ang II levels, both systemically and intrarenally, aminopeptidase A acts to tonically control blood pressure and to moderate Ang II-induced renal injury.
{"title":"The role of aminopeptidases in angiotensin peptide processing","authors":"Wayne R Fitzgibbon","doi":"10.1016/j.cophys.2026.100898","DOIUrl":"10.1016/j.cophys.2026.100898","url":null,"abstract":"<div><div>Plasma and tissue levels of angiotensin peptides are regulated by their formation and metabolism by peptidases. Aminopeptidases A and N process Ang II to Ang III and Ang III to Ang IV, respectively, peptides which may have the same physiological action as, or counterbalance the action of, Ang II. In this minireview, other pathways for the processing of both Ang I and Ang II by aminopeptidases will be outlined. Further, the differential processing of Ang I and Ang II by different cell types comprising the renal glomerulus will be discussed. Importantly, by playing a role in the regulation of Ang II levels, both systemically and intrarenally, aminopeptidase A acts to tonically control blood pressure and to moderate Ang II-induced renal injury.</div></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"47 ","pages":"Article 100898"},"PeriodicalIF":1.9,"publicationDate":"2026-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146077832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-05DOI: 10.1016/j.cophys.2025.100897
Mohammad A Ali, Basem Elbarouni
Sex differences in chronic total occlusion (CTO) percutaneous coronary intervention (PCI) reflect biological, procedural, and systemic factors. Females are older, carry greater comorbidity, and are underrepresented in trials. Despite similar procedural success, they experience higher rates of bleeding and target vessel revascularization complications, yet adjusted long-term outcomes are comparable to males. These findings highlight the need for equitable trial representation, tailored bleeding-avoidance strategies, and improved understanding of sex-related vascular and plaque biology in CTO PCI.
{"title":"Sex differences in outcomes for percutaneous coronary intervention and chronic total occlusions","authors":"Mohammad A Ali, Basem Elbarouni","doi":"10.1016/j.cophys.2025.100897","DOIUrl":"10.1016/j.cophys.2025.100897","url":null,"abstract":"<div><div>Sex differences in chronic total occlusion (CTO) percutaneous coronary intervention (PCI) reflect biological, procedural, and systemic factors. Females are older, carry greater comorbidity, and are underrepresented in trials. Despite similar procedural success, they experience higher rates of bleeding and target vessel revascularization complications, yet adjusted long-term outcomes are comparable to males. These findings highlight the need for equitable trial representation, tailored bleeding-avoidance strategies, and improved understanding of sex-related vascular and plaque biology in CTO PCI.</div></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"47 ","pages":"Article 100897"},"PeriodicalIF":1.9,"publicationDate":"2026-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146077831","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-02DOI: 10.1016/j.cophys.2025.100896
Emily Nordmann , Jill RD MacKay
Lecture capture is frequently justified as an inclusive technology, yet its alignment with Universal Design for Learning (UDL) in post-pandemic practice has not been empirically considered. We conducted a scoping review of post-pandemic lecture capture research, identifying 12 studies that considered live lecture recording in higher education. Using the UDL guidelines as an analytic framework, we found that lecture capture primarily supports Engagement and, to a lesser extent, Representation through flexible access, replay and player controls. Action and Expression and higher-level executive functions were rarely addressed. Demographic reporting was limited, with few analyses for disabled, neurodivergent or commuting students. We argue that lecture capture is necessary, but insufficient as a sole adjustment for inclusive design and prioritise future research.
{"title":"Lecture capture as Universal Design for Learning: a post-pandemic scoping review","authors":"Emily Nordmann , Jill RD MacKay","doi":"10.1016/j.cophys.2025.100896","DOIUrl":"10.1016/j.cophys.2025.100896","url":null,"abstract":"<div><div>Lecture capture is frequently justified as an inclusive technology, yet its alignment with Universal Design for Learning (UDL) in post-pandemic practice has not been empirically considered. We conducted a scoping review of post-pandemic lecture capture research, identifying 12 studies that considered live lecture recording in higher education. Using the UDL guidelines as an analytic framework, we found that lecture capture primarily supports Engagement and, to a lesser extent, Representation through flexible access, replay and player controls. Action and Expression and higher-level executive functions were rarely addressed. Demographic reporting was limited, with few analyses for disabled, neurodivergent or commuting students. We argue that lecture capture is necessary, but insufficient as a sole adjustment for inclusive design and prioritise future research.</div></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"47 ","pages":"Article 100896"},"PeriodicalIF":1.9,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146037892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-25DOI: 10.1016/j.cophys.2025.100895
Steven P Jones, Helen E Collins
The composite of changes sustained by the left ventricle during pathologic and physiologic stimuli is known as ventricular remodeling. These changes involve alterations to individual cells, the surrounding matrix, and overall ventricular structure and function. Following myocardial infarction, ventricular remodeling involves partial tissue repair and ultimately determines long-term survival. Biological sex contributes to diverging responses in post-infarction ventricular remodeling and survival, with young female animals having less remodeling post-injury compared with male animals, yet women have reduced long-term survival. Over the last two decades, evidence indicates that sex-dependent differences impact most processes that contribute to post-infarction remodeling, including extracellular matrix remodeling, inflammation, and cardiomyocyte homeostasis. In addition, there are differences in the transcriptional landscape and cellular composition of male and female hearts. Despite these well-established sex-dependent differences, mechanistic advancements lag. Furthermore, cardiovascular treatments are not yet optimized based on sex. Sex hormones are proffered as the explanation for differences; however, studies that remove the influence of sex hormones still show sex-dependent changes, which suggests hormone-independent contributors. Outside of pathological remodeling in response to infarction, the female heart often undergoes physiological remodeling that does not occur in males: pregnancy. During pregnancy, rapid remodeling and reversion occur, which creates a unique, natural template to study aspects of sex-dependent differences in ventricular remodeling. Therefore, this review summarizes fundamental differences in the ventricular myocardium between sexes and highlights emerging areas that contribute to sex-dependent changes in ventricular remodeling.
{"title":"Sex and ventricular remodeling","authors":"Steven P Jones, Helen E Collins","doi":"10.1016/j.cophys.2025.100895","DOIUrl":"10.1016/j.cophys.2025.100895","url":null,"abstract":"<div><div>The composite of changes sustained by the left ventricle during pathologic and physiologic stimuli is known as ventricular remodeling. These changes involve alterations to individual cells, the surrounding matrix, and overall ventricular structure and function. Following myocardial infarction, ventricular remodeling involves partial tissue repair and ultimately determines long-term survival. Biological sex contributes to diverging responses in post-infarction ventricular remodeling and survival, with young female animals having less remodeling post-injury compared with male animals, yet women have reduced long-term survival. Over the last two decades, evidence indicates that sex-dependent differences impact most processes that contribute to post-infarction remodeling, including extracellular matrix remodeling, inflammation, and cardiomyocyte homeostasis. In addition, there are differences in the transcriptional landscape and cellular composition of male and female hearts. Despite these well-established sex-dependent differences, mechanistic advancements lag. Furthermore, cardiovascular treatments are not yet optimized based on sex. Sex hormones are proffered as the explanation for differences; however, studies that remove the influence of sex hormones still show sex-dependent changes, which suggests hormone-independent contributors. Outside of pathological remodeling in response to infarction, the female heart often undergoes physiological remodeling that does not occur in males: pregnancy. During pregnancy, rapid remodeling and reversion occur, which creates a unique, natural template to study aspects of sex-dependent differences in ventricular remodeling. Therefore, this review summarizes fundamental differences in the ventricular myocardium between sexes and highlights emerging areas that contribute to sex-dependent changes in ventricular remodeling.</div></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"47 ","pages":"Article 100895"},"PeriodicalIF":1.9,"publicationDate":"2025-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145977634","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-24DOI: 10.1016/j.cophys.2025.100894
Christopher L Schaich , Ashish K Khanna , Mark C Chappell
Sepsis and septic shock are associated with high mortality rates and constitute the primary cause of death in intensive care units worldwide. Activation of the circulating renin-angiotensin-aldosterone system (RAAS) is an early event, and elements of the RAAS, including renin, Angiotensinogen, and ACE2, may be predictive of worse outcomes and higher mortality that reflect a failure to increase the circulating levels of the vasopressor Ang II. Emerging evidence suggests that dipeptidyl peptidase III (DPP3) is involved in the metabolism of Ang II, and higher DPP3 in septic shock may contribute to lower Ang II tone. The current review considers the role of a dysfunctional RAAS to maintain blood pressure and adequate tissue perfusion in septic shock.
{"title":"Novel aspects of the renin-angiotensin-aldosterone system in septic shock","authors":"Christopher L Schaich , Ashish K Khanna , Mark C Chappell","doi":"10.1016/j.cophys.2025.100894","DOIUrl":"10.1016/j.cophys.2025.100894","url":null,"abstract":"<div><div>Sepsis and septic shock are associated with high mortality rates and constitute the primary cause of death in intensive care units worldwide. Activation of the circulating renin-angiotensin-aldosterone system (RAAS) is an early event, and elements of the RAAS, including renin, Angiotensinogen, and ACE2, may be predictive of worse outcomes and higher mortality that reflect a failure to increase the circulating levels of the vasopressor Ang II. Emerging evidence suggests that dipeptidyl peptidase III (DPP3) is involved in the metabolism of Ang II, and higher DPP3 in septic shock may contribute to lower Ang II tone. The current review considers the role of a dysfunctional RAAS to maintain blood pressure and adequate tissue perfusion in septic shock.</div></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"47 ","pages":"Article 100894"},"PeriodicalIF":1.9,"publicationDate":"2025-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145977636","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-22DOI: 10.1016/j.cophys.2025.100893
Wenxi An, Iris Z Jaffe
Endothelial cell mineralocorticoid receptor (EC-MR) is a central regulator of vascular dysfunction beyond its classical renal role. This review summarizes recent advances in our understanding of how EC-MR disrupts vasomotor control via endothelial sodium channel activation, endothelial nitric oxide synthase dysregulation, and glycocalyx injury, amplifies inflammation and oxidative stress via serum and glucocorticoid-induced protein kinases-1, NLRP3, and mitochondrial reactive oxygen species, and drives fibrosis and remodeling via transforming growth factor-β (TGF-β). Through these mechanisms, EC-MR contributes to diabetes- and obesity-related vascular disease, acute and chronic kidney injury, and to new disorders, including ocular, skin, and hypoxic pulmonary diseases, reproductive vascular physiology, cerebrovascular dysfunction, COVID-19 vasculopathy, and cardiac dysfunction. Evidence from preclinical and clinical studies supports both traditional and novel nonsteroidal mineralocorticoid receptor antagonists as potential therapies for these additional indications and suggests endothelial biomarkers to guide translation.
{"title":"Emerging roles for endothelial mineralocorticoid receptor in disease pathogenesis: potential new indications for mineralocorticoid receptor antagonism","authors":"Wenxi An, Iris Z Jaffe","doi":"10.1016/j.cophys.2025.100893","DOIUrl":"10.1016/j.cophys.2025.100893","url":null,"abstract":"<div><div>Endothelial cell mineralocorticoid receptor (EC-MR) is a central regulator of vascular dysfunction beyond its classical renal role. This review summarizes recent advances in our understanding of how EC-MR disrupts vasomotor control via endothelial sodium channel activation, endothelial nitric oxide synthase dysregulation, and glycocalyx injury, amplifies inflammation and oxidative stress via serum and glucocorticoid-induced protein kinases-1, NLRP3, and mitochondrial reactive oxygen species, and drives fibrosis and remodeling via transforming growth factor-β (TGF-β). Through these mechanisms, EC-MR contributes to diabetes- and obesity-related vascular disease, acute and chronic kidney injury, and to new disorders, including ocular, skin, and hypoxic pulmonary diseases, reproductive vascular physiology, cerebrovascular dysfunction, COVID-19 vasculopathy, and cardiac dysfunction. Evidence from preclinical and clinical studies supports both traditional and novel nonsteroidal mineralocorticoid receptor antagonists as potential therapies for these additional indications and suggests endothelial biomarkers to guide translation.</div></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"47 ","pages":"Article 100893"},"PeriodicalIF":1.9,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145977635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-16DOI: 10.1016/j.cophys.2025.100890
Minna Luo, Hang Xiao
Natural polyphenols have been widely studied for their anti-inflammatory properties in inflammatory bowel disease (IBD). However, recent research has also highlighted their critical role in redox imbalance in IBD. This review highlights recent advances in understanding the redox-modulating effects of selected polyphenols, including curcumin, resveratrol, epigallocatechin-3-gallate (EGCG), quercetin, and anthocyanins. Preclinical studies and clinical trials demonstrate that these compounds exert their protective effects through multiple redox-related mechanisms, such as scavenging reactive oxygen species, activating antioxidant pathways like Nrf2/HO-1, enhancing endogenous antioxidant enzymes, and modulating redox-sensitive inflammatory signaling cytokines in IBD. However, translation to clinical application is challenged by issues such as dual antioxidant/pro-oxidant roles, inconsistent biomarker reporting, lack of serum-based measurements in animal studies, and poor mechanical understanding regarding redox dysfunction. Future research should prioritize standardized redox endpoints and mechanistic validation to advance polyphenol-based therapies. Collectively, the current evidence supports the therapeutic potential of polyphenols as redox-targeted adjuncts in IBD.
{"title":"Curcumin, resveratrol, and other polyphenols in regulating redox imbalance in inflammatory bowel disease","authors":"Minna Luo, Hang Xiao","doi":"10.1016/j.cophys.2025.100890","DOIUrl":"10.1016/j.cophys.2025.100890","url":null,"abstract":"<div><div>Natural polyphenols have been widely studied for their anti-inflammatory properties in inflammatory bowel disease (IBD). However, recent research has also highlighted their critical role in redox imbalance in IBD. This review highlights recent advances in understanding the redox-modulating effects of selected polyphenols, including curcumin, resveratrol, epigallocatechin-3-gallate (EGCG), quercetin, and anthocyanins. Preclinical studies and clinical trials demonstrate that these compounds exert their protective effects through multiple redox-related mechanisms, such as scavenging reactive oxygen species, activating antioxidant pathways like Nrf2/HO-1, enhancing endogenous antioxidant enzymes, and modulating redox-sensitive inflammatory signaling cytokines in IBD. However, translation to clinical application is challenged by issues such as dual antioxidant/pro-oxidant roles, inconsistent biomarker reporting, lack of serum-based measurements in animal studies, and poor mechanical understanding regarding redox dysfunction. Future research should prioritize standardized redox endpoints and mechanistic validation to advance polyphenol-based therapies. Collectively, the current evidence supports the therapeutic potential of polyphenols as redox-targeted adjuncts in IBD.</div></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"47 ","pages":"Article 100890"},"PeriodicalIF":1.9,"publicationDate":"2025-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145884654","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-16DOI: 10.1016/j.cophys.2025.100892
Tania Akter Jhuma, Tao Yang
The gut microbiota is a highly modifiable factor that influences disease susceptibility, progression, and response to therapy. In hypertension, it shapes systemic inflammation, metabolite production, and renin–angiotensin system (RAS) activity. The RAS is a central regulator of blood pressure, fluid balance, and vascular function, and many antihypertensive therapies target this system. Understanding the interactions between the gut microbiota and RAS offers new opportunities to develop microbiota-targeted interventions that modulate RAS activity, improve blood pressure control, reduce organ damage, and support personalized treatment strategies. In this review, we summarize current knowledge on the bidirectional communications between the gut microbiota and RAS in the context of hypertension.
{"title":"Crosstalk between gut microbiota and the renin–angiotensin system in hypertension","authors":"Tania Akter Jhuma, Tao Yang","doi":"10.1016/j.cophys.2025.100892","DOIUrl":"10.1016/j.cophys.2025.100892","url":null,"abstract":"<div><div>The gut microbiota is a highly modifiable factor that influences disease susceptibility, progression, and response to therapy. In hypertension, it shapes systemic inflammation, metabolite production, and renin–angiotensin system (RAS) activity. The RAS is a central regulator of blood pressure, fluid balance, and vascular function, and many antihypertensive therapies target this system. Understanding the interactions between the gut microbiota and RAS offers new opportunities to develop microbiota-targeted interventions that modulate RAS activity, improve blood pressure control, reduce organ damage, and support personalized treatment strategies. In this review, we summarize current knowledge on the bidirectional communications between the gut microbiota and RAS in the context of hypertension.</div></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"47 ","pages":"Article 100892"},"PeriodicalIF":1.9,"publicationDate":"2025-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145926320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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