Author

Alyssa M. Richards

Purdue University West Lafayette

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Physiology· 2 Pharmacology & Toxicology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:mouse· 3 Assay:imaging· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Research Focus:development & morphogenesis· 1 Research Focus:differential expression· 1 Research Focus:host-pathogen & immune response· 1

Frequent Co-Authors

Conner C. EarliD· 3 shared Craig J. GoergeniD· 3 shared Areli Jannes S. JavieriD· 2 shared Larry Wayne MarkhamiD· 2 shared Niharika Narra· 2 shared Steven S. WelciD· 2 shared Abigail D. CoxiD· 1 shared Akanksha AgrawaliD· 1 shared

Activity by Year

2024-2026 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 39 mutual co-author links

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3 shared papersPhysiology

Conner C. EarlORCID

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3 papers

Recent·Most cited

Positive allosteric modulator of SERCA pump NDC-1171 attenuates cardiac functional decline in mouse model of Duchenne muscular dystrophy

Niharika Narra, Alyssa M. Richards, Conner C. Earl, Abigail D. Cox, Russell S. Dahl, Wendy A. Koss, Craig J. Goergen

NDC-1171, a SERCA pump modulator, preserves cardiac function in DMD mice but does not improve skeletal muscle function.

Function · Sep 10, 2026Peer-reviewedPharmacology & Toxicology

Empagliflozin preserves cardiac function and modulates metabolism in a mouse model of Duchenne muscular dystrophy

B. Zeidler, Connor R Thomas, John P. Salvas, Areli Jannes S. Javier, Alyssa M. Richards, Linda A. Bean, Conner C. Earl, Akanksha Agrawal, Niharika Narra, Li‐Fan Zeng, Carol A. Witczak, Joshua R. Huot, Il‐man Kim, Meena S. Madhur, Mark C. Kowala, , Steven S. Welc

This study shows empagliflozin improves cardiac function and mitochondrial health in a mouse model of Duchenne muscular dystrophy.

bioRxiv · Mar 14, 2026 · PreprintPhysiology

Functional cardiac consequences of β-adrenergic stress-induced injury in the mdx mouse model of Duchenne muscular dystrophy

Conner C. Earl, Areli J. Javier, Alyssa M. Richards, Larry W. Markham, Craig J. Goergen, Steven S. Welc

This paper introduces a method using low-dose isoproterenol to enhance cardiac dysfunction in mdx mice, showing increased myocyte injury, fibrosis, and reduced ventricular function compared to wild-type mice.

bioRxiv · Apr 15, 2024 · PreprintPhysiology